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FEDERAL STATE BUDGETARY EDUCATIONAL DEPARTMENT OF HIGHER PROFESSIONAL EDUCATION

MOSCOW STATE ACADEMY OF VETERINARY MEDICINE AND BIOTECHNOLOGY them. K. I. SKRYABINA

____________________________________________________________

V. N. Denisenko, Yu. S. Kruglova

VETERINARY

IMMUNOPATOLOGY

LECTURE

MOSCOW, 2011

UDC 619:616-097.3(07)

Kruglov immunopathology. Lecture. - Moscow.: FGBOU VPO MGAVMiB them. , 2011, 30 p.

The paper presents materials reflecting the protective reactions of the body's immune system, as well as immunodeficiency states. The role of allergic and autoimmune reactions, as well as immune complexes in the development of the pathological process in non-communicable animal diseases is shown.

The lecture is intended for students of full-time, part-time and part-time (evening) faculties of veterinary medicine, students of the advanced training faculty and practicing veterinarians.

Reviewer: Petrov A. M., doctor wind. Sci., professor of Moscow State Academy of Medical and Biological Safety named after A.I. .

Gavrilov V. A., doctor wind. Sci., professor of Moscow State Academy of Medical and Biological Safety named after A.I.

The lecture was approved at a meeting of the educational and methodological commission of the Faculty of Veterinary Medicine (Minutes No.

1. Introduction

2. Protective reactions of the body's immune system

3. Immunodeficiency states

4. Allergy

5. Diseases of animals, the pathogenesis of which is caused by allergic reactions

6. Immunological tolerance

INTRODUCTION

The immune system maintains the body's homeostasis. It recognizes genetically alien substances, neutralizes and eliminates them, and prevents re-entry into the body. However, in some cases, substances produced by immune responses can damage host cells and tissues and thus cause disease in animals.

Of the immune pathologies among animals, weakening of immune reactivity (immunodeficiencies) and allergies (atopy) are more common than others. Allergies are atypical immune reactions that are characterized by an increase, complication and acceleration of the immune response.

In recent years, the role of immune reactions in the pathology of animals has increased markedly. Immunodeficiency states play a leading role in the wide spread of animal diseases caused by opportunistic pathogens.

Allergic reactions are involved in the pathogenesis of anaphylactic shock, serum sickness, acute glomerulonephritis, allergic rhinitis, bronchitis, dermatitis. They complicate the course of many infectious and parasitic diseases.

The development of allergies is associated with damage to the lymphoid tissue, a violation of the mechanisms of the body's immunological reactivity, a change in the antigenic properties of host tissues, and the presence of an excessive amount of immune complexes.

A significant role in the allergization of animals is assigned to environmental pollution, the emergence of new synthetic substances, food preservatives and additives.

Mechanisms of immune defense

The immune system is represented by a set of organs, tissues and cells that react to the ingestion of genetically alien substances - antigens. Microorganisms and their metabolic products, foreign proteins, polysaccharides, nucleoproteins, insect toxins, plant pollen have antigenic properties.

The morphological basis of the immune system is lymphoid tissue. It forms the parenchyma of the spleen, thymus and lymph nodes. Accumulations of lymphocytes are found under the mucous membrane of the intestines, pharynx, bronchi, genitourinary system, salivary and lacrimal glands and other tissues. In the blood of different animal species, lymphocytes make up from 21 to 65% of all leukocytes.

Some lymphocytes circulate from the blood to the tissues and vice versa. No lymphocytes were found in the brain tissue of healthy animals.

In addition to lymphocytes, mononuclear phagocytes in the form of tissue macrophages and blood monocytes, as well as eosinophils, neutrophils and mast cells, take part in the implementation of immune reactions.

Cells of the immune system synthesize substances - interleukins, lymphokines, etc., which play the role of mediators in immune reactions.

Immune reactions develop after the introduction of an antigen into the body. An active physiological immune response includes the recognition of an invading antigen as a foreign substance, its disintegration by macrophages, and the transmission of antigenic information to immunocompetent cells. As a result of the reaction of the latter, humoral and cellular mechanisms of immunity are formed.

humoral mechanism The immune response is associated with the formation of antibodies. Antibodies are synthesized by plasma cells, which are formed from B-lymphocytes. In the first phase of the immune response, high molecular weight IgM is synthesized, followed by IgG and IgA. Class A immunoglobulins penetrate the surface of the mucous membranes, combine with secretory proteins and become resistant to the action of the proteolytic enzymes pepsin and trypsin.

Mucosal protection is provided mainly by secretory IgA. In recent years, it has been proven that a significant part of secretory antibodies belong to IgG. Antibodies play a leading role in the antibacterial and antitoxic protection of the body.

Class E immunoglobulins are found in the blood serum of healthy animals in small amounts. They play an important role in the formation of immunopathological reactions, in particular allergies. In animals suffering from allergies, their content in the blood serum is higher than in healthy ones.

Natural resistance. Congenital nonspecific factors of natural resistance play an important role in protecting the body. They provide general protection to the body. The action of natural resistance factors is aimed at neutralizing all or several antigens. Nonspecific protection is provided by cellular and humoral factors.

Cellular factors of natural resistance include phagocytic cells - neutrophils and monocytes. Humoral factors of natural resistance are complement and properdin systems, lysozyme, interferons, lactoferrins, and other substances.

Factors of natural resistance and immunity interact with each other in the protective reactions of the body.

Diseases of the immune system

Lymphoid tissue can be affected by physical, chemical and biological factors. Diseases of the immune system manifest themselves in the form of a decrease in the body's immunological reactivity (immunodeficiencies), atypical immune reactions (allergies) or lack of immune reactions (tolerance).

Immunodeficiencies

Immunodeficiency states are characterized by a decrease in the body's immune reactivity. They are divided into primary and secondary. Colostral and age-related immunodeficiencies are considered separately.

Distinguish deficiency of cellular (T-dependent), humoral (B-dependent) immunity and combined immunodeficiency.

Humoral immunity deficiency- hypo - and agammaglobulinemia is characterized by a decrease in the synthesis or an increase in the destruction of immunoglobulins. At the same time, the concentration of B-lymphocytes can be reduced to a complete absence, the content of IgG and IgA is at a low level. In other cases, the content of B-lymphocytes remains normal, but they synthesize only IgM.

Immune globulin deficiency has been established in cattle, pigs, sheep, fur-bearing animals, and dogs: IgA deficiency has been described in Beagles and Shar-Peis, and IgM deficiency in Dobermans.

Deficiency in cell-mediated immunity characterized by a low content of T-lymphocytes. More often it is a consequence of damage to the thymus and a violation of the differentiation of lymphoid tissue.

Pathogenesis . Primary immunodeficiencies are associated with a genetically determined insufficiency in the development of immunocompetent cells. In animals, due to breeding work, this form of immunodeficiency is rare.

Secondary immunodeficiency states develop as a result of damage to immunocompetent cells by biological, chemical and physical factors. They are noted after animals have been ill with infectious and parasitic diseases, after the use of certain drugs, with radioactive exposure, with a deficiency in the diet of protein, vitamins, microelements, after surgical operations, with excessive exploitation, as a result of stress.

Colostral immunodeficiency states are noted in newborn animals. Their development is associated with a violation of the technology of drinking colostrum, its insufficient amount, a decrease in the concentration of immune factors in colostrum and a violation of the ability to absorb colostrum by the offspring. Of particular importance is the time of the first feeding of colostrum. Thus, newborn calves absorb the bulk of colostral immunoglobulins in the first 3-4 hours of life.

By the third day of life, they completely lose the ability to absorb colostrum immunoglobulins. The ability of calves to assimilate colostrum lymphocytes in the first hours of life has also been proven. The transition of cells contained in colostrum from the intestines to the calf's blood occurs due to a change in the structure of the walls of the digestive tube, the appearance of "hatches" in it.

Combined immunodeficiency is characterized by impaired cellular and humoral immunity. X-linked combined immunodeficiency has been described in the literature in Bassets.

In young cattle, an age-related deficiency of humoral and cellular immunity factors has been established. In calves at 14-20 days of age, it is associated with depletion of colostral and insufficient synthesis of their own immunoglobulins. The decrease in immunological reactivity at 5-6 months of age is associated with a change in the diet and conditions of animals.

Immunodeficiency in old animals is explained by atrophy of the thymus.

Clinical picture immune deficiency is manifested by an increase in the incidence in animals. Diseases are caused by both pathogenic and opportunistic pathogens. They have a chronic relapsing course, are difficult to treat and often end in death or forced slaughter. In young animals, the respiratory and digestive systems are usually affected, in cows - the genitals. Surgical and accidental wounds suppurate, heal poorly, and pustular lesions of the skin and mucous membranes are also noted.

In females and cats, mucopurulent discharge from the vagina is observed, in males - from the prepuce.

Laboratory research . The presence of an immunodeficiency state is confirmed by laboratory studies of indicators characterizing the body's immune reactivity.

A general clinical blood test reveals an absolute and relative decrease in the concentration of lymphocytes in immunodeficient animals.

More objectively reflect the state of immune reactivity data on the percentage of undifferentiated (null), B - and T-lymphocytes. In cows, it is 42, 24 and 34%, respectively. A decrease in the proportion of immunocompetent cells (T- and B-lymphocytes) indicates the presence of immunodeficiency.

In immunodeficient animals, a decrease in the concentration of immunoglobulins of classes G, M and A, complement, lysozyme, properdin is also noted. After immunization, these animals have reduced antibody titers to the vaccine antigen.

Stable indicators of insufficiency of cellular immunity is a decrease in swallowing and, especially, digesting activity of neutrophils and monocytes.

Treatment and prevention . Treatment of immune deficiency is aimed at eliminating etiological factors and normalizing the mechanisms of immune reactivity.

The fight against immune deficiency includes selection work, providing animals with a complete diet, compliance with zoohygienic requirements for keeping, and regular exercise. Take preventive measures against infectious diseases in a timely manner.

Of the medicinal preparations for therapeutic and prophylactic purposes, immunomodulators are used, which normalize the processes of proliferation and differentiation of lymphoid tissue. These include T-activin, B-activin, fosprenil, thymogen, etc.

The immunological reactivity of the body is normalized by the use of vitamin preparations, protein hydrolysates, microelements. To stimulate cellular immunity, it is recommended to use levamisole.

For the prevention of colostral immunodeficiency, it is necessary to properly feed colostrum to newborn animals, especially in the first days of life.

Allergy

The term "allergy" (from the Greek allos - another, ergon - action) was first introduced by Pirke in 1904. Allergy is characterized by an increase and perversion of the body's immune responses with repeated injections of the antigen. Antigens that cause allergic reactions are called allergens.

There are exo- and endoallergens. Exoallergens - foreign proteins, complex compounds, waste products of microorganisms, protozoa, insect toxins, drugs, plant pollen, artificially synthesized substances. They enter the body from the external environment.

Endoallergens (autoallergens) are contained and formed in the body. Allergies are caused by tissues of the barrier organs (brain, testicles, vitreous body, thyroid gland) when the barriers are damaged. The properties of allergens are acquired by host proteins denatured under the influence of physical, chemical and biological factors. Heart tissues in rheumatic myocarditis, kidneys in chronic nephritis, liver in chronic hepatitis, bronchi in chronic bronchitis, skin in burns and frostbite cause allergic reactions.

Classification of allergic reactions

The first classification of allergies was proposed by R. Cook in 1930. In 1969, P. Jell and R. Coombs developed a classification that takes into account the nature of all immunopathologies.

R. Cook's classification takes into account the time of appearance of the body's reaction after the repeated introduction of the allergen. According to this classification, all allergic reactions are divided into two groups: immediate hypersensitivity (HHT) and delayed hypersensitivity (DTH) types.

GNT reactions develop no later than 2 hours, and more often a few minutes after the repeated introduction of the allergen.

HRT develops 24 hours later and later after repeated exposure to the antigen. Delayed-type hypersensitivity reactions include infectious allergies in tuberculosis, brucellosis.

The classification of P. Gell and R. Coombs covers all known forms of immunopathology. According to this classification, all allergic reactions are divided into four types.

I type of (anaphylactic) refers to GNT. It is characterized by the fact that during primary contact with the allergen, the body produces a large amount of specific class E immunoglobulins. Normally, JgE is contained in a small amount. These immunoglobulins with their Fc fragments are fixed on receptors located on the membranes of mast cells and basophils. When the allergen enters the body again, it is bound by two IgE molecules fixed on mast cell membranes. As a result, mast cells are activated, accompanied by the release of biologically active substances from it - histamine, serotonin, bradykinin. These substances are inflammatory mediators.

An allergic reaction of type I forms the basis of the pathogenesis of such diseases as anaphylactic shock, allergic dermatitis (urticaria), allergic rhinitis, conjunctivitis, bronchitis and atopic bronchial asthma, drug intolerance, Quincke's edema.

II type of - cytotoxic. It is characterized by immune lysis of the body's own cells in which the antigenic structure of cell membranes is changed. A change in the antigenic properties of cells occurs when viruses, bacteria, and their metabolic products adhere to them. The antigenic properties of cell membranes can be changed by some medicinal substances - heparin, sulfonamides, barbiturates, acetylsalicylic acid, penicillin antibiotics. These cells stimulate the production of IgG and IgM antibodies. These antibodies form immune complexes with cell antigens, which activate the complement system. As a result of activation, the last components of the complement system (C8- and C9-) acquire the properties of enzymes. The latter lyse cells with altered antigenic structure. Currently, autoimmune reactions of the body are associated with an allergic reaction of type II. An allergic reaction of type II underlies the pathogenesis of autoimmune hemolytic anemia, leukopenia, thrombocytopenia, autoimmune atrophic gastritis, autoimmune pancreatitis, and chronic active hepatitis.

III type of due to excessive formation of immune complexes: antigen-antibody and activation of the complement system. The formation of immune complexes is a physiological form of binding and excretion of antigens from the body. Normally, immune complexes are metabolized by phagocytosis and excreted from the body in the urine. In violation of the catabolism of immune complexes, which is noted with their excess, type III allergy develops.

Immune complexes are formed when exo- and endoantigens bind to precipitating IgG and IgM antibodies. Hyperimmune sera, gamma globulins, bacterial and viral metabolic products, some drugs, as well as modified host cells can serve as antigens.

Hardly soluble complexes formed with an excess of polyvalent antigens - lipopolysaccharides and proteins - have the greatest damaging effect.

The damaging effect of these complexes is associated with biologically active substances that are formed during complement activation (C3 and C5 convertases). In addition, immune complexes activate cells carrying Fc and C receptors. At the same time, neutrophils and macrophages secrete lysosomal enzymes, mast cells - histamine.

Immune complexes are deposited more often on blood vessels where there is increased pressure or areas of turbulent blood flow - the capillaries of the renal glomeruli, the choroid of the eye, the skin, the serous and synovial membranes. In this regard, they cause such immune complex diseases as glomerulonephritis, serum sickness, uveitis, allergic vasculitis, rheumatoid arthritis.

With the local formation of immune complexes, the Arthus reaction develops. It is observed in actively or passively immunized animals after subcutaneous injection of antigen or antibodies, and is characterized by vascular necrotic processes. After 4-10 hours, vasculitis develops at the injection site, then, after the destruction of the basement membrane of capillaries by lytic factors, blood cells and the above-described biologically active substances pass into the extravascular space. They cause a vascular reaction, necrosis and tissue lysis. The Arthus reaction is often noted in hyperimmunization of animals.

IV type (cellular) refers to delayed-type hypersensitivity (DTH). It is characterized by a local inflammatory reaction at the site of contact of sensitized lymphocytes with the antigen.

With intradermal administration of the antigen, the first signs of DTH are erythema, edema, which appears after 6-8 hours and after 24-48 hours they reach a peak.

The DTH reaction begins with monocytes entering the site of contact with the antigen. They phagocytize the antigen and provide information about it to T cells. T cells recognize the antigen and secrete a soluble factor that stimulates the release of histamine and serotonin from mast cells. These mediators increase the permeability of blood capillaries, which contributes to the entry of monocytes and macrophages into the focus, which phagocytize the antigen. In the chronic course of HRT, a granuloma is formed, which consists of macrophages, lymphocytes, plasma cells, neutrophils and eosinophils.

Animal diseases, the pathogenesis of which is caused by allergic reactions

Immediate type hypersensitivity (ITH) can clinically manifest itself as systemic or local lesions of the animal's organs. Systemic pathologies include anaphylactic shock (anaphylaxis), local ones include hay fever, allergic dermatitis, rhinitis, conjunctivitis, bronchitis, bronchial asthma, and food intolerance.

Anaphylactic shock

Anaphylactic shock in animals develops as a result of a type I allergic reaction (GHT). The disease proceeds quickly with the involvement of the main body systems and, in the absence of medical assistance, can be fatal. Anaphylactic shock occurs in all animal species.

Etiology. In animals, anaphylactic shock can develop after reimmunization against bacterial and viral diseases, with repeated use of antibiotics, sulfanilamide and other drugs, with the use of hyperimmune sera and donor blood immunoglobulins. There is an anaphylactic reaction to feed. Poisons of bees, wasps, hornets, fungal spores can act as allergens.

Pathogenesis. After the initial entry of the allergen into the animal's body, antibodies are synthesized that belong to the IgE class. IgE antibodies with their Fc fragments are fixed on the corresponding receptors of mast cells and basophils. The indicated stage of the allergic reaction proceeds without the manifestation of clinical signs and pathochemical changes.

When the antigen is re-introduced into the body of a sensitized animal, it binds to antibodies of the IgE class. This forms an antigen-antibody complex fixed on mast cells and basophils.

These immune complexes stimulate the release of a mediator by mast cells and basophils - histamine, serotonin, eosinophilic and neutrophilic chemotactic factors. At the same time, the synthesis of new mediators is launched - platelet activating factor, prostaglandins, lysosomal enzymes, leukotrienes.

Histamine causes contraction of smooth muscles, increased vascular permeability and blistering, increased secretion of mucus by goblet cells, dilation of arterioles and capillaries.

Serotonin causes spasm of the vessels of the heart, brain, lungs, kidneys, contraction of smooth muscles.

ProstaglandinsF2 a stimulate the release of mediators by mast cells.

platelet activating factor activates platelet aggregation and their release of serotonin, stimulates bronchospasm, increases vascular permeability and blistering.

Clinical picture . Clinical signs of anaphylactic shock appear immediately after repeated contact with the allergen or after a few minutes. The time of their manifestation depends on the quality of the allergen and on the method of its introduction into the animal's body. In particular, with intravenous administration, signs of HIT appear during the procedure. Anaphylactic shock occurs systemically, i.e., with the involvement of the respiratory system, cardiovascular system, liver, skin and mucous membranes, and intestinal damage.

The main clinical signs are manifested in the form of rhinitis, conjunctivitis, asthma, pruritus. There are tonic and clonic convulsions, spasms of the smooth muscles of the bronchi, bronchioles, intestines, swelling of the mucous membranes and increased secretion of the intestinal glands, bronchi. Expansion and increased permeability of blood vessels leads to pulmonary edema, overflow of the liver with blood. There is shortness of breath, involuntary excretion of feces and urine, bradycardia, copious outflow of mucus from the nasal passages.

In cattle, continuous ruminant movements, the release of a foamy liquid from the oral cavity, and acute timpania of the scar are observed. Horses are characterized by anemia of the mucous membranes, dilated nostrils, labored wheezing, heart failure, and pulmonary edema.

The disease is extremely acute and, in the absence of immediate veterinary care, ends in the death of the animal from suffocation, heart and lung failure.

Pollinosis (hay fever)

Pollinosis is an allergic disease that occurs according to the first type of allergy. The clinical manifestation of hay fever is characterized by seasonal allergic rhinitis, allergic conjunctivitis, allergic inflammation of the paranasal sinuses, allergic bronchitis and allergic dermatitis.

Clinical manifestations of pollinosis largely depend on the method of introducing the allergen into the animal's body. In particular, with the parenteral administration of a large amount of the same allergens that, when inhaled, cause a local reaction, anaphylactic shock may occur.

Etiology . The main etiological factor of hay fever is the pollen of wind-pollinated plants. About 60 species of plants are known in the world, the pollen of which causes hay fever. The pollen of these plants is extremely small, so it is easily carried by the wind over long distances. The penetration of pollen into the body of animals and humans occurs with the help of the enzyme contained in it. The disease is seasonal; the first period of rise is spring, associated with the flowering of trees, the second is summer, associated with the flowering of meadow grasses, the third is autumn, associated with the flowering of weeds.

In addition to plant pollen, allergens are mold spores that infect straw, hay, and grain waste. The clinical picture of hay fever can be caused by some drugs, the excrement of house mites contained in house dust, the epidermis of the skin and animal hair.

Allergic inflammation in some cases affects both the skin and mucous membranes of the eyes and respiratory tract, in others - separate systems.

Allergic dermatitis

Allergic dermatitis, the pathogenesis of which is caused by a type I allergic reaction, is characterized by hyperacute inflammation of the skin and subcutaneous tissue.

The disease proceeds in the form of urticaria or inflammatory vascular edema. It can occur in combination with allergic rhinitis and bronchitis.

Etiology . The disease develops quickly, within a few minutes, after repeated contact of the animal with the allergen. An allergen can enter the body by the oral or parenteral route. An allergic reaction can develop after skin contact with an allergen. Allergens are epidermal cells, feces of mites, certain types of food, fungal spores, plant pollen, bee and insect venoms, toxins and metabolic products of microorganisms, antibiotics, hormones, vitamins, food colorings, preservatives and antioxidants. In dogs, horses and cattle, allergic dermatitis occurs after the use of protein preparations, vaccines, after blood transfusions and in some infectious diseases. In pigs, they appear as a result of intensive feeding with fishmeal. Contact allergic dermatitis can be caused by harnesses, collars, care items, ointments, sprays.

Pathogenesis . The disease is associated with degranulation of mast cells caused by the IgE-antigen immune complex and the release of a large number of inflammatory mediators into the blood.

Clinical picture . With the manifestation of allergic dermatitis in the form of urticaria, rashes can appear on different parts of the body. The rash is accompanied by severe itching of the skin. Urticaria is characterized by the formation of blisters on the skin with uneven raised borders, surrounded by a zone of edema and hyperemia. The blisters may coalesce.

Histological examination of the affected areas of the skin shows loosening of collagen fibers, dilation of blood vessels and the presence of perivascular infiltrates consisting of lymphocytes, eosinophils and neutrophils. After the action of the allergen is eliminated, the rashes disappear within 24 hours.

With the clinical manifestation of allergic dermatitis in the form of inflammatory vascular edema, hyperemia and edema of individual sections of soft tissues are noted, edema can spread to the mucous membranes. Inflammatory vascular edema, which captures large areas and extends not only to the dermis, but also to the subcutaneous tissue, is called Quincke's edema. Local dermatitis can occur upon contact with an allergen. When contact with the allergen is eliminated, the signs of allergic dermatitis disappear within 12-24 hours. With allergic dermatitis, blood tests indicate eosinophilia and leukopenia.

allergic rhinitis

Allergic rhinitis is an inflammation of the mucous membranes of the nose that occurs after inhalation of an allergen. The disease may be seasonal or occur regardless of the season.

Etiology . The development of seasonal rhinitis is due to contact with plant pollen. The cause of year-round rhinitis are allergens with which the animal is in constant contact. These include mold spores, the epidermis of other animal species, house dust, and industrial waste. Allergic rhinitis often affects animals suffering from other forms of allergies.

It is believed that allergens with a size of 10-100 microns settle on the nasal mucosa and cause allergic rhinitis, smaller allergens reach the bronchi and can cause allergic bronchitis and asthma.

Pathogenesis . Under the action of enzymes of the nasal mucosa, especially lysozyme, the outer shell of pollen, spores and other allergens is destroyed, which leads to the release of proteins, the molecular weight of which is. Allergens bind to mast cells, located in large numbers around the entire submucosal layer, which are sensitized by homologous antibodies of the IgE class. Allergen-specific antibodies of the IgE class are found not only on mast cells, but also on basophils. Histamine and other inflammatory mediators, which are secreted by mast cells and basophils, cause edema and eosinophilic infiltration of the nasal mucosa and sometimes the conjunctiva of the eyes. Edema of the mucous membrane of the turbinates contributes to the layering of a secondary infection and the development of sinusitis and edema.

Allergic (eosinophilic) bronchitis and bronchial asthma

The disease is characterized by the presence of cough, copious secretion of bronchial secretions containing a large number of eosinophils. Asthma (suffocation) is understood as the increased sensitivity of the bronchi to irritants, which leads to their spasms and labile obstruction.

Etiology . The main role in the development of allergic bronchitis and bronchial asthma is played by allergens - plant pollen, fungal spores, dust, smoke, volatile chemicals, certain drugs, foods, waste products of bacteria.

Predisposing factors are genetically determined instability of cell membranes, violation of the relationship between the regulators of the immune system. Low temperature and high humidity also have an effect.

Secondary bronchospasms are noted in chronic bronchitis, bronchopulmonary infection.

Pathogenesis The disease is caused by an allergic reaction of type I, sometimes type II.

Clinical picture . Clinical signs of the disease appear immediately after inhalation of the allergen. They are characterized by choking cough, sneezing, expiratory dyspnea, wheezing, conjunctivitis, and vomiting may occur. In the presence of bronchial asthma, there is a release of viscous mucus and swelling of the bronchial mucosa, which leads to asthma attacks. Auscultation revealed wet and dry rales, whistles.

On the x-ray, the lung has increased transparency, the diaphragm is flattened. In chronic cases, the bronchial tree is clearly expressed, interstitial and alveolar blackouts are noted.

With the help of laboratory tests, an increased content of eosinophils in the blood and a large number of them in the bronchial secretion are detected.

food allergy

An allergic reaction of an immediate type can develop to foods.

Most often, some animal proteins (milk, pork, fish, poultry) and flour products - oatmeal, wheat, etc. cause allergies. Chicken eggs can also serve as food allergens.

Food allergies can appear locally and systemically. In the first case, only the alimentary canal is affected. There is an edematous reaction on the mucous membrane of the oral cavity. If the allergenic food is swallowed, the mucous membrane of the esophagus and stomach swells, vomiting begins. With a systemic manifestation of food allergy, the response develops within a few minutes and can lead, along with damage to the digestive tract, to an attack of bronchial asthma, Quincke's edema, and even to anaphylactic shock. Hypersensitivity to allergenic food can manifest itself in the form of hives, swelling of the eyelids, tongue and larynx.

Diagnosis of diseases, the pathogenesis of which is caused by allergies

Itype

Diagnosis of allergic pathologies includes the analysis of anamnestic data, clinical studies, the study of blood, sputum and other materials obtained from sick animals. Intradermal and contact tests are also carried out. Certain diagnostic value are the results of the use of antihistamines. When analyzing the anamnestic data, they find out which substances cause an allergic reaction. Pay attention to the dynamics of the pathological process. Type I allergy is characterized by the rapid appearance of clinical signs of the disease and their disappearance within 1-2 days after the elimination of contact with the allergen.

The ineffectiveness of the traditional treatment of inflammatory processes with the use of antimicrobial drugs and the positive effect when using antihistamines indicate the allergic nature of the disease.

Diseases, the pathogenesis of which is caused by type I allergy, are extremely acute and acute. Their clinic is characterized by aseptic inflammation and swelling of the skin, subcutaneous tissue, mucous membranes of the oral cavity, intestines and alimentary canal. At the same time, the same allergens, depending on the method of introduction into the body and the dose, can cause both local lesions and anaphylactic shock. The greatest danger to the life of animals is anaphylactic shock, as it is accompanied by heart failure and pulmonary edema. With skin lesions for type I allergies, edema, itching, and urticaria are characteristic.

When diagnosing allergies, the key point is the definition of the allergen. For this purpose, intradermal and contact tests, or an oral test are used.

Intradermal test . The suspected allergen is injected intradermally in a volume of 0.1 or 0.05 ml. Before setting the sample, the hair is shaved, and the skin is treated with ethyl alcohol. The input material must be sterile. Bacteriological filters are used to sterilize thermolabile substances, and thermostable substances are autoclaved.

A positive reaction in type I allergy is characterized by the formation of swelling and redness or blisters at the injection site of the allergen after a few minutes. These signs disappear without treatment after 24-48 hours.

contact test is less sensitive. During its setting, a swab moistened with the test substance is attached to the skin with a patch. With a positive reaction, the skin at the site of contact with the allergen turns red after 1-2 hours.

oral test . When it is placed on the mucous membranes of the oral cavity, the allergen is applied in the form of an aerosol. The mucous membrane of the oral cavity swells and turns red 3-5 minutes after the oral test.

Laboratory research. Hematological studies reveal eosinophilia in allergic people. Microscopy of azure-eosin-stained smears in sputum of animals with allergic bronchitis and asthma reveals an accumulation of eosinophils.

Obtaining a positive result with the use of antihistamines has a certain diagnostic value.

Differential diagnosis is aimed at eliminating diseases caused by viruses, bacteria, fungi, physical and chemical factors.

Treatment

First, it is necessary to exclude the entry of the allergen into the body of the animal. Treatment is carried out comprehensively, with the use of drugs that affect all parts of the pathological process and taking into account the clinical manifestation of the disease.

Prescribe drugs that inhibit the release of histamine, bradykinin, serotonin by mast cells and reduce the sensitivity of body cells to them.

In the presence of spasms of the bronchi, hypersecretion of the bronchial glands and coronary insufficiency, which occurs with anaphylactic shock, allergic bronchitis and bronchial asthma, bronchodilators and drugs that block M-cholinergic receptors and stimulate α- and β-adrenergic receptors are also used.

The names of drugs and doses for different types of animals are given in the table.

Doses of drugs for the treatment of allergies in different animal species

Name of the drug	Release form	Methods of administration
Prednisolone is a synthetic glucocorticoid. It inhibits the degranulation of mast cells and basophils and the release of histamine, bradykinin, etc. into the blood.	tab. 0.001 and 0.005 g; amp. 3% - 1 ml		0.25-1 mg/kg IV, IM or orally; May be 600-800 mg (1.3-1.7 mg/kg) per 450 kg animal IM or orally. Then reduce the dose to 0.4 mg/kg every other day (200 mg per animal) and until discontinued.	1-4 mg/kg orally, IM or orally;	0.2-1 mg/kg IV or IM	0.2-1 mg/kg IV or IM	0.25 - 10 mg / kg orally or parenterally; To suppress the inflammatory process, the initial dose is 0.5-1 mg / kg 2 r / day peros. After 5–7 days, 1–2 mg/kg every other day orally and reduce dose until discontinued; Substitution treatment 0.25 mg/kg daily peros; With allergies, prednisolone succinate (water-soluble) 0.5-1 mg / kg 2 r / day in / in and / m; For shock, 5-10 mg/kg, repeat after 1, 3 and sometimes 6 hours.	1-4 mg/kg daily IV, IM, or orally divided into 2 daily doses; Pulse therapy 50-100 mg/kg IV.
Dexamethasone is a synthetic long acting glucocorticoid. Pronounced anti-inflammatory and anti-allergic action. 35 times more active than cortisone and 7 times more active than prednisolone.	tab. 0.0005 and 0.001 g; amp. 4 mg 1 ml	In/articular	0.01-0.05 mg/kg 1 r/day i/v, i/m and orally; 5-20 mg per animal	0.01-0.05 mg/kg 1 r/day i/v, i/m, s/c and orally; 5-20 mg per animal	0.05-2 mg/kg IM or IV; 1-10 mg per animal	0.05-2 mg/kg IM or IV; 1-10 mg per animal; Piglets 0.5 mg	0.05-2 mg/kg; As an anti-inflammatory --0.05 mg/kg 1-2 r/day orally; In shock, cerebral edema 1-2-4 mg/kg IV, repeat after 4-6 hours. Then 0.5 mg / kg 2-3 r / day during the day. Further to reduce a dose before the termination; Topically (intrabursally) 2-4 mg 1 time per day up to 3 days	0.1-0.5 mg / kg IV, s / c or / m; Topically (intrabursally) 2-4 mg 1 time per day up to 3 days
Atropine sulfate. A drug that blocks m-cholinergic receptors and, thus, neutralizes the action of acetylcholine. It has an antispasmodic effect, reduces the tone of the smooth muscles of the bronchi, intestines, bladder and suppresses the secretion of the bronchial, nasopharyngeal and digestive glands	amp. 0.1% - 1 ml; tab 0.005 g; 1% eye ointment; eye films		0.04-0.15 mg/kg	0.04-0.15 mg/kg	0.1-0.15 mg/kg	0.1-0.15 mg/kg	0.2-1 mg/kg 1-2 r/day s/c; For premedication before anesthesia 0.02-0.05 mg / kg s / c. in / m and / in. with an increase in salivation, sinus bradycardia, the indicated dosage is repeated until the effect is achieved or s p / day orally; In case of poisoning with alkyl phosphate 0.2-2 mg / kg, ¼ dose IV, the rest s / c or / m	0.1-1 mg/kg s.c.
Adrenaline hydrochloride (epinephrine) is an analogue of endogenous catecholamine. The drug relaxes the smooth muscles of the bronchi and iris, a histamine antagonist, enhances glycogenolysis, increases blood sugar levels, increases the pulse rate when administered intravenously, has a vasoconstrictive effect and increases systolic blood pressure. In veterinary practice, it is used for anaphylaxis, to stimulate the heart. With s / c administration of the drug, the effect occurs later, after 5-10 minutes. When administered orally, it has no effect.	amp. 0.1% - 1 ml vial 10 ml 0.1%			0.5-1 ml / 40 kg diluted 1:1000 s / c or / m		0.5-3 ml / 50 kg diluted 1:1000 s / c or / m		In case of anaphylaxis in a dilution of 1:10000 at a dose of 0.01-0.02 mg / kg slowly intravenously, intramuscularly or s / c, or intratracheally a double dose
Euphyllin is a myotropic bronchodilator. It causes a decrease in the intracellular concentration of calcium ions and relaxation of the muscles of the bronchi, reduces pressure in the pulmonary circulation, improves blood circulation in the heart, kidneys and brain.	amp 24% - 10 ml for i / m amp 2.4% - 10 ml for IV		1-4 mg/kg s.c.	1-4 mg/kg s.c.	4-6 mg/kg s.c.	4-6 mg/kg s.c.	Inside 25 mg / kg IM 25-50 mg/kg in 10-20 ml of 40% glucose solution; IV 2.5-5 mg/kg	S / c 3-5 mg / kg
Diphenhydramine is an antihistamine drug. Inhibits histamine at H1 receptor sites. It has a sedative, anticholinergic, antitussive and antiemetic effect. In veterinary medicine, it is used as an antihistamine, for the treatment of itching, especially associated with allergic reactions, and for the prevention of stress during transportation of animals.	tab. 0.02; 0.03; 0.05g; amp. 1% - 1 ml	s / c, inside, topically (skin, in the form of eye drops, on the next vol.)	0.25-1 mg/kg IV or IM	0.5-1 mg/kg IV or IM	0.5-0.6 mg/kg	0.5-0.6 mg/kg	2-4 mg/kg IM	2-4 mg/kg IM
amp 1% - 1 ml	Doses inside 1.5-2 times more

It should be noted that the use of the above drugs allows you to transfer the disease from the acute stage to the stage of remission. It does not eliminate the etiological factors and does not exclude, with repeated contact with allergens, the manifestation of the disease in an acute form.

A stable remission can be obtained by completely eliminating the contact of the animal with the allergen or by reducing the body's sensitivity to the latter.

In order to reduce the sensitivity of the animal's body to the allergen, the method of hyposensitization is used. When it is performed, first, with the help of intradermal tests, it is determined which substance is an allergen for the animal. Then the specified substance in small doses for a long time is injected into the body of the animal parenterally.

This method gives positive results in the presence of 1-2 allergens. With multiple allergies, when allergens are a large number of different substances, it is ineffective.

Prevention allergies includes compliance with sanitary and hygienic requirements in keeping animals, selection work, timely and effective treatment of diseases, exclusion from the diet of substances that exhibit allergenic properties.

For the prevention of drug allergies, the method of fractional administration (desensitization according to Bezredko) is used. When using this method, 1/10 part of the drug dose is first administered to the animal, then, after 1.5-2 hours, the remaining 9/10 parts are administered. This method eliminates the clinical manifestation of an allergic reaction.

Autoimmune reactions

Autoimmune reactions are characterized by the formation of antibodies or sensitized lymphocytes to the body's own antigens. The pathogenesis of these reactions develops according to type II allergy. Currently, there are several causes that cause the appearance of autoimmunity.

One of them is the release of "hidden" antigens, that is, antigens that are isolated from immunocompetent cells by hemato-tissue barriers. In particular, "hidden" antigens are the internal components of cells, the vitreous body, pancreatic parenchyma, testis tissue, brain, thyroid gland. When the hemato-tissue barriers are damaged, the "hidden" antigens are released and trigger the body's immune response. For example, when emulsified tissue of a previously removed testis is administered parenterally to the host, after some time damage to the tissues of a healthy testis occurs. An autoimmune reaction also explains the sympathetic ophthalmia that occurs in a healthy eye with a penetrating injury to the other eye.

Self antigens can be formed in the body as a result of protein denaturation by physical, chemical or biological factors. Such denaturation can be observed as a result of a burn, tissue frostbite, exposure to drugs and microbial toxins.

Autoimmune reactions can occur when antigens are introduced into the body that are similar to the tissue proteins of the macroorganism. For example, it has been established that antibodies to bovine hemoglobin are present in the blood serum of animals with abscesses caused by corynebacteria. Similar properties were also found in the antigens of streptococcus, myofibrils of the heart and kidney tissues. The properties of autoantigens can be possessed by complex compounds that are formed when proteins of a macroorganism combine with the waste products of microorganisms.

Autoimmune processes are more common in senile age, since with aging there is an accumulation of mutant forms of somatic cells.

And, finally, the cause of autoimmune reactions can be the insufficiency of the immune system, namely, a violation of its ability to identify its own antigens from foreign ones. It is believed that one of the reasons for this deficiency is the deficiency of various forms of T - and B-lymphocytes.

Autoimmune processes play a role in the pathogenesis of autoimmune hemolytic anemia, hepatitis, pancreatitis, gastritis, myocarditis, rheumatoid arthritis, systemic lupus erythematosus, etc.

For diseases in the pathogenesis of which an autoimmune component is involved, eosinophilia, accelerated ESR, is characteristic. In the blood serum, antibodies to self antigens and C-reactive protein are detected.

For the treatment of animals with the above diseases, along with other necessary drugs, it is recommended to use glucocorticosteroids, cytostatics and other immunosuppressants.

Autoimmune hemolytic anemia

The disease is characterized by severe anemia, splenomegaly, swollen lymph nodes, jaundice. Described in dogs and cats; females are more commonly affected.

Etiology . The main etiological factor is a change in the antigenic structure of the erythrocyte cell wall, as a result of which they acquire the properties of autoantigens.

Pathogenesis . Autoantigens of the erythrocyte wall induce the production of autoantibodies of the IgM and IgG classes to them.

Antibodies form immune complexes (AG-AT) with erythrocytes, which cause classical activation of the complement system. The 8th and 9th components of the complement system have lytic properties. They cause lysis of red blood cells. Macrophages of the spleen and lymph nodes are also involved in the process of hemolysis. As a result of massive hemolysis, a large amount of free hemoglobin is released. Part of it is converted by phagocytes of the liver and lymph nodes into free bilirubin, and part is excreted from the body with urine.

Clinical picture . Animals are depressed, there is shortness of breath, anorexia, vomiting, fever. The mucous membranes due to severe anemia have a porcelain appearance, the spleen and peripheral lymph nodes are greatly enlarged in size. There is yellowness of the sclera, dark brown urine, dark feces. The number of heartbeats is increased. There is blood in the anterior chamber of the eye (black eye).

In laboratory blood tests, severe anemia is detected, the concentration of erythrocytes decreases to 1-2 x1012/l, the osmotic resistance of erythrocytes is reduced. Spherical erythrocytes (spherocytes) and reticulocytes are found.

With the help of immunological tests, immunoglobulins G and M classes and C3 (the third complement component) are detected on the surface of erythrocytes.

Diagnostic the presence of anemia, an increase in the size of the spleen and lymph nodes, the detection of spherical erythrocytes and IgM, IgG and C3 on erythrocytes is important.

Treatment autoimmune hemolytic anemia is aimed at suppressing the body's immune responses. To reduce phagocytic activity and inhibition of antibody synthesis, prednisone is prescribed at the rate of 1 mg/kg of body weight 2 times a day. After seven days of treatment, the dose of prednisolone is constantly reduced until it is completely canceled. In some cases, sick animals must take prednisolone throughout their lives at the rate of 0.5 mg/kg of body weight every three days. In cases where the use of glucocorticoids is not enough, cytostatics are prescribed. It is recommended to use cyclophosphamide at a dose of 1.5 mg/kg for dogs weighing more than 25 kg; 2.0 mg/kg for animals weighing 6-24 kg; 2.5 mg/kg - for animals weighing less than 5 kg. The drug is taken orally 4 times a week for three weeks.

If there are signs of oxygen deficiency, oxygen therapy is carried out.

Prevention disease is aimed at eliminating etiological factors. It is necessary to treat infectious, invasive and non-infectious diseases in a timely manner, to exclude from the use of drugs that cause damage to red blood cells. Animals with autoimmune anemia are excluded from breeding.

Autoimmune atrophic gastritis

This is a rare disease, which is characterized by atrophy of the gastric mucosa and loss of secretory ability.

Etiology . Autoimmune gastritis is associated with a genetic predisposition. Older dogs are more commonly affected. Atrophic gastritis is based on autoimmune processes (Twedt & Magne, 1986). The body produces antibodies that damage the main, accessory and parietal cells of the fundic glands of the stomach with their subsequent loss.

Pathogenesis . With this disease, atrophy of the mucous membrane occurs, which leads to a decrease in the number of acid-producing cells. As a result, the volume of gastric juice and hydrochloric acid decreases. The pH level becomes higher than 3.5. All this can lead to an overgrowth of the microflora in the small intestine, poor absorption, chronic diarrhea and weight loss.

Clinical picture . Atrophic gastritis is characterized by chronic intermittent vomiting, often for several months. The vomit contains mucus, bile, pieces of undigested food. Belching and anorexia are possible, sometimes abdominal pain (the position of the praying).

Diagnosis . Gastroscopy reveals thinning of the mucosa with a small amount of uneven flattened ridge folds, increased mucus in the lumen of the stomach. The blood vessels of the submucosal layer are clearly visible.

Biopsy of the mucosa provides important information. Microscopically observed loss of glandular tissue, infiltration of plasma cells, as well as varying degrees of fibrosis.

An x-ray can provide additional information. Autoimmune atrophic gastritis must be differentiated from secondary atrophic gastritis, tumors.

Forecast careful. Complete recovery usually does not occur. Chronic atrophic gastritis is classified as a precancerous condition of the stomach; against the background of this disease, precancerous changes such as intestinal metaplasia and dysplasia of the epithelium of the gastric mucosa, as well as hyperproliferation of the epithelium of the gastric mucosa, which contribute to the development of tumors, often develop.

Treatment . A bland diet is required. Feeding should be frequent, in small portions. Preferably meat, not cereals, it is better to choose a hypoallergenic diet. Dry food can drown out the symptoms of the disease for a while, as they do not require a large amount of gastric juice and are easily digested.

If necessary, prescribe preparations of gastric juice (pepsin, hydrochloric acid). Antibiotics may be necessary for excessive development of pathogenic microflora and chronic diarrhea. Assign tylosin 20 mg/kg body weight 2 times a day.

Glucocorticoids are prescribed with caution. Although they suppress the autoimmune process, they can also cause stomach ulcers by stimulating the production of hydrochloric acid. Azathioprine is recommended.

Chronic active hepatitis

It is a progressive autoimmune disease characterized by focal necrosis of hepatocytes in the limiting lamina of the acinus.

Clinical picture . Apathy, anorexia, mild jaundice, weakness. Later, polyuria, polydipsia, jaundice, emaciation, melena and vomiting appear. Ultimately, portal hypertension, ascites, cirrhosis or fibrosis of the liver, hepatoencephalopathy develop.

Diagnosis . To make a diagnosis, it is necessary to conduct a biochemical study of blood serum. A strong, 15-fold increase in the level of serum alanine aminotransferase, as well as alkaline phosphatase, bilirubin, is observed. The clearance of bromsulphthalein is reduced. Hypergammaglobulinemia and hypoalbuminemia are also characteristic.

Differential diagnosis is carried out with chronic progressive hepatitis. Unlike chronic active hepatitis, it is a relatively benign hepatitis, with little tendency to cirrhosis or fibrosis, which may resolve spontaneously. In contrast, chronic active hepatitis often leads to liver failure and death. A biopsy is necessary for differential diagnosis, as macroscopically the liver may appear unchanged. The presence of periportal necrosis, as well as a significant increase in the level of transferases, hypergammaglobulinemia, and unsuccessful therapy confirm the diagnosis of chronic active hepatitis. It is also necessary to differentiate the disease from chronic cholangitis, liver granulomas, copper storage disease (in Bedlington Terriers, Dobermans).

Forecast doubtful.

Treatment . Diet and multivitamins are essential. After clinical improvement, glucocorticoids are prescribed. Prednisolone is used at a dose of 1-2 mg/kg with a gradual dose reduction after clinical improvement. It can be combined with azathioprine at a dose of 1 mg/kg.

Found in cats chronic cholangiohepatitis caused by immune-mediated factors. The course of the disease resembles primary biliary cirrhosis. The initial bacterial infection is thought to cause an immune-mediated hepatocellular injury or bile duct destruction that exacerbates the initial injury. Clinical signs of the disease are similar to those found in acute cholangiohepatitis (anorexia, weight loss, weakness, drowsiness, vomiting, often hepatomegaly, sometimes fever). In the blood, neutrophilia is observed with a shift of the nucleus to the left. Biochemical abnormalities include an increase in the concentration of total bilirubin.

Treatment . Assign ursodeoxycholic acid 10-15 mg/kg orally 1 time per day. Prednisolone 2.2-6.6 mg/kg once a day with a gradual dose reduction to 2-4 mg/kg once every two days as a long-term maintenance therapy.

Autoimmune pancreatitis

Autoimmune pancreatitis is an inflammation of the pancreas, which is based on the production of antibodies against its own pancreatic tissue. Dogs get acute pancreatitis more often than cats.

Etiology . The same causes that cause non-immune pancreatitis can lead to the production of autoantibodies. This is a diet saturated with fats, mechanical trauma, drugs (sulfamethazole, azathioprine, corticosteroids, furosemide, chlorthiazide, estrogens, sulfonamides). Cushing's syndrome results in high levels of cortisol in the blood, which causes acute pancreatitis. In cats, pancreatitis can occur after treatment with drugs of the tetracycline group. Pancreatitis can be caused by infectious agents (parvovirus, toxoplasma, etc.). The relationship of hyperlipidemia, hypercalcemia and hypovolemia with the development of pancreatitis has been established. These phenomena can cause ischemia of the organ, activate and increase the production of enzymes by the pancreas.

Pathogenesis . The basis of the pathogenesis of autoimmune pancreatitis is a change in the antigenic structure of pancreatic cells caused by physical, chemical, mechanical, biological and other factors. Antibodies are produced on cells with an altered antigenic structure. Antibodies form an antigen-antibody complex with altered cells, which activates the complement system, the 8th and 9th components of which have lytic activity. Tissue cytolysis is noted. At the same time, pancreatic enzymes, in particular trypsin, are activated. Trypsin activates two other enzymes. It is an elastase that cleaves the elastic fibers of the blood vessels, leading to bleeding, thrombosis and ischemia, and, in addition, digests the interstitial connective tissue. The second enzyme is phospholipase A, which cleaves acinar cell membranes, which enhances the release of enzymes. Acute inflammation and pain begin, leading to hypovolemia and shock. Trypsin also activates bradykininogen, which eventually leads to extensive circulatory collapse. The release of lipase leads to fat necrosis.

Against the background of hypovolemia and ischemia of the pancreas, Clostridia microorganisms begin to multiply, which can lead to peritonitis.

The possible end result of the acute form of the disease is irreversible shock and disseminated intravascular coagulation. In the chronic form of pancreatitis, the inflammatory process gradually leads to the complete replacement of exocrine tissue with fibrous tissue, which is manifested by exocrine pancreatic insufficiency and the development of diabetes mellitus.

Clinical picture . Autoimmune pancreatitis is usually severe. Observe anorexia, depression, dehydration, abdominal pain, vomiting. Feces are frequent and plentiful, with a sour smell, diarrhea is possible. Intestinal peristalsis is increased, it is swollen. Cats often have jaundice, due to the fact that they share a common pathway for bile and pancreatic secretions. At the beginning of the disease, there may be an increase in temperature up to 40 ° C, and then, as shock develops, on the contrary, a drop in body temperature.

In addition to the symptoms described above, hypocalcic tetany, shortness of breath, cyanosis, pulmonary edema, hyperglycemia, hemorrhagic diathesis, blood in the feces and vomit (signs of DIC syndrome) can be observed.

In the chronic form of pancreatitis, despite the fact that the animal eats, it loses weight, the owners complain of a dull coat and incessant molting.

Diagnosis . The disease must be differentiated from an abscess, from hemorrhagic gastoenteritis, hepatitis, intestinal perforation, acute gastritis.

Hematological analysis reveals an increase in hematocrit (a consequence of dehydration), neutrophilic leukocytosis with a shift of the nucleus to the left. An increase in the level of serum amylase and lipase may indicate diseases of the liver and kidneys, that is, it does not always indicate the presence of pancreatitis. Nevertheless, a threefold excess of the physiological values ​​of these indicators is certainly significant. In the ascitic fluid, a large amount of amylase and lipase are also found.

When examining feces, a large number of fat droplets are noted, which indicates a violation of the digestion of fats. On ultrasound, the pancreas is diffusely enlarged, has irregular outlines, and mixed echogenicity. Two days before the study, special attention should be paid to the prevention of gas formation, since in animals with pancreatitis the intestines are swollen. On the radiograph (it is desirable to conduct a study with contrast), darkening in the right hypochondrium, ventral or right-sided displacement of the duodenum 12, displacement in the caudal direction of the transverse sections of the colon.

Forecast with edematous pancreatitis, more common in cats, favorable or cautious. In acute necrotizing pancreatitis, the prognosis is uncertain.

Treatment . To prevent hypovolemia and metabolic acidosis, 5% sodium bicarbonate solution or Ringer's solution is administered intravenously. To neutralize lipase in the blood, contrical is prescribed. When vomiting - metoclopramide hydrochloride (raglan) intramuscularly or subcutaneously at a dose of 0.2-0.4 mg / kg every 6-8 hours (R. Kirk. D. Bonagura, 2005).

To reduce further secretion of pancreatic enzymes, it is important to stop eating in the first 2-5 days. When appetite appears, parenteral or enteral nutrition is prescribed. To suppress pancreatic secretion, anticholinergic drugs (atropine sulfate), intravenous glucagon at a dose of 0.3 mg/kg, intravenous insulin at a dose of 0.5 IU/kg are recommended (J. Simpson, 2003). Assign enzyme preparations (creon, panzinorm).

To stop the development of primary and secondary infections, broad-spectrum antibiotics are always prescribed, such as gentamicin, ampicillin, amoxicillin, chloramphenicol (J. Simpson, 2003), or baytril, which penetrates well into the pancreatic tissue, intramuscularly at a dose of 2.5 mg /kg every 12 hours for dogs (R. Kirk. D. Bonagura, 2005).

Corticosteroids are used with great caution. They themselves can cause acute pancreatitis. They should be used only in conditions close to shock, for example, prednisolone at a dose of 6-10 mg / kg. To relieve pain, antispasmodics can be used - no-shpu, papaverine, baralgin or analgesics, for example, butorphanol at a dose of 0.2-0.4 mg / kg every 6 hours subcutaneously to dogs and cats (R. Kirk. D. Bonagura, 2005 ).

In the initial stages of the disease, a diet high in carbohydrates (boiled rice) and low in fat and protein is required.

Immune complex diseases

The pathogenesis of immune complex diseases is associated with type III allergic reaction. The formation of immune complexes, consisting of precipitating antibodies of the IgG and IgM classes and antigens in quantities exceeding the body's ability to metabolize them, is noted with the use of hyperimmune serum, hyperimmunization of the body, and chronic diseases.

Of the immune complex diseases, glomerulonephritis, serum sickness, the Arthus phenomenon and rheumatoid arthritis are of the greatest practical importance in veterinary practice.

Glomerulonephritis

This is inflammation of the glomeruli, which is caused by immune complexes and antibodies. The disease is characterized by the manifestation of hypersensitivity in the vascular glomeruli of the kidneys, the proliferation of the endothelium and the thickening of the membranes of their capillaries. Glomerulonephritis has an acute and chronic course.

Etiology . The disease often has an infectious-allergic nature, less often it is not associated with infectious agents. In animals, glomerulonephritis occurs after infectious diseases, immunization, or the use of hyperimmune serum and specific immunoglobulins; can develop as a result of chronic uroinfection, pustular skin lesions, with purulent sinusitis, sinusitis caused by streptococci and staphylococci.

The cause of the disease can be drugs, especially some antibiotics and vitamins, toxins of organic and inorganic origin, plant pollen. Contribute to the disease of animals with glomerulonephritis adverse environmental factors - low temperature and high humidity. There is information about the genetic predisposition of animals to the disease glomerulonephritis.

Pathogenesis . The pathogenetic basis of glomerulonephritis is an allergic reaction of type III. The leading role in its development is assigned to immune reactions that develop on the basement membrane of the capillaries of the renal glomeruli with the participation of circulating immune complexes. In some cases, autoantibodies to kidney tissues play this role.

The formation of complexes consisting of antigen and antibodies is a normal process. Subsequently, these complexes are metabolized by mononuclear phagocytes. When an excessive amount of antigen enters the body, some of the complexes formed are deposited on the basement membrane of the capillaries. Immune complexes activate the complement system. In this case, the fifth and third components of the complement system after activation (C5 and C3) acquire chemotactic properties. They attract neutrophils to the lesion and stimulate phagocytosis. Enzymes released from neutrophil lysosomes during phagocytosis damage the basement membrane of the capillaries of the renal glomeruli. As a result of membrane damage, erythrocytes and plasma proteins appear in the urine, blood coagulates in the capillaries, and platelet aggregation is noted.

In the chronic course of glomerulonephritis, morphological changes in the glomeruli can be characterized by sclerosis of individual capillaries, massive deposition of immune complexes on their basement membranes, proliferation of mesangial cells with their penetration into the lumen of the capillaries.

Clinical picture . Symptoms of glomerulonephritis appear 12-14 days after immunization of those who have recovered from an infectious disease or exposure to other etiological factors. The disease can occur in two forms - cyclic and latent.

The cyclic form develops rapidly and proceeds rapidly. There is general depression, refusal to feed, body temperature can rise by 1-1.50C, the kidney area is painful on palpation and percussion. For the cyclic form of glomerulonephritis, urinary, edematous and hypertensive, nephrotic syndromes are characteristic. Urine acquires the color of meat slops, its density is reduced.

In laboratory studies of urine, hematuria, proteinuria, the presence of hyaline and erythrocyte cylinders are noted. Hematological parameters are characterized by leukocytosis, accelerated ESR.

In the blood serum, the content of urea, creatinine, cholesterol is increased, the alkaline reserve is lowered, the clearance of endogenous creatinine is lowered.

With a favorable course of the disease and effective treatment, these symptoms disappear after 2-3 weeks. If left untreated, the disease can become chronic.

With a latent form, glomerulonephritis occurs without pronounced clinical signs. Nephrotic and hypertensive syndromes are absent. Clinically, the disease is manifested by slight shortness of breath and edema. Urinary syndrome is mild, it is characterized by nocturia and microhematuria.

The latent form of acute glomerulonephritis, in the absence of rational treatment, often turns into chronic glomerulonephritis.

Under the influence of adverse environmental factors, in particular stress, low temperatures and high humidity, which lead to a decrease in the body's natural resistance, chronic glomerulonephritis may worsen. Especially often exacerbations are observed in autumn and spring.

Chronic glomerulonephritis ends with a secondary wrinkled kidney.

Diagnostics cyclic glomerulonephritis is carried out in a complex. Diagnostic value is the appearance of signs of the disease 12-14 days after an infectious disease or immunization, the use of hyperimmune serum, as well as severe hematuria. The disease develops acutely and is characterized by soreness and an increase in the size of the kidneys. Urine has the color of meat slops, the content of erythrocytes in it prevails over the number of leukocytes. There is acute renal failure, uremic and nephrotic syndromes. The echogram shows an expansion of the cortical layer and a decrease in its echogenicity. Puncture biopsy of the kidneys in animals with glomerulonephritis reveals an increase in the size of the glomeruli (80-100%), narrowing of the lumen of their capillaries, an increase in the thickness of the mesangial matrix, and an abundance of neutrophilic leukocytes. Along the basement membranes of the capillaries of the glomeruli and in the mesangium, using special test systems, granular lumpy deposits are found, consisting of class G and C3 immunoglobulins (the third complement component).

The latent form is characterized by the absence of pronounced clinical signs, proteinuria, microhematuria, and the presence of edema.

In a chronic course, the echogenicity of the cortical layer increases.

Treatment glomerulonephritis is aimed at eliminating contact with antigens, suppressing microorganisms and an allergic inflammatory reaction in the renal glomeruli, and stimulating diuresis.

Antibiotics, sulfa drugs, nitrofurans, quinolones, fluorochtnolones are used to suppress microflora. Preference is given to active, non-nephrotoxic drugs that are excreted unchanged from the body by the kidneys.

From antibiotics, klaforan, ampioks, chloramphenicol, tetracycline are used, from nitrofuran compounds - furadonin and furagin, from the group of quinolones - nitroxoline (5-NOC), from fluoroquinolones - norfloxacin (nolicin).

To suppress the inflammatory allergic reaction, prednisolone or dexamethasone and drugs with an immunosuppressive effect (cyclophosphamide) are prescribed. Stimulation of diuresis is carried out with the help of furosemide.

Serum sickness

Serum sickness is caused by immune complexes and is characterized by high fever, urticaria, lymphadenitis, arthritis, glomerulonephritis, and heart failure.

Etiology . Serum sickness develops 8-14 days after the administration of large doses of foreign hyperimmune serum or other protein preparations to animals.

Pathogenesis Serum sickness develops according to type III allergic reaction, that is, with the participation of immune complexes. When a large amount of a heterogeneous protein is introduced into the body, the synthesis of antibodies to it begins earlier than the metabolism and excretion of the drug from the body. Antibodies form immune complexes with foreign protein residues. Immune complexes, especially those consisting of positively charged proteins and antibodies, are deposited on the basement membranes of the capillaries of the renal glomeruli, the synovial membrane, the skin, and the choroid of the eyeball.

In the future, as in glomerulonephritis, complement activation occurs with the formation of C5 and C3, neutrophil chemotaxis, phagocytosis with the release of lysosomal enzymes that damage the basement membranes of capillaries.

Damage to the basement membranes of capillaries is accompanied by the development of an aseptic inflammatory reaction.

Clinical picture . The clinical picture of serum sickness is characterized by high fever, urticaria, glomerulonephritis, arthritis, uveitis, pericarditis, inflammation of the lymph nodes, heart failure. Inflammatory processes develop aseptically.

Diagnostics . When diagnosing, anamnestic data on the use of a sick animal 8-14 days before the onset of clinical signs of hyperimmune serum disease or other protein drugs are important. The diagnosis is confirmed by the presence of immune complexes in biopsy specimens.

Treatment . In the treatment of serum sickness, antihistamines and anti-inflammatory drugs (diphenhydramine, prednisolone, dexamethasone) are used. Symptomatic treatment is also carried out with the use of diuretic and cardiac drugs.

Arthus phenomenon

The disease is a model of local damage to body tissues by immune complexes. It develops after intradermal administration of a homologous antigen to a sensitized animal. The Arthus phenomenon is noted in hyperimmunization of experimental animals, in reimmunization against infectious diseases, and also in the bites of blood-sucking insects.

Clinical picture the Arthus phenomenon is characterized by the development within an hour at the site of intradermal, sometimes intramuscular injection of the antigen of exudative-hemorrhagic inflammation. In the future, the foci of inflammation are encapsulated and turn into nodules, which undergo necrosis and lysis.

Pathogenesis diseases are associated with the formation of immune complexes in the walls of small vessels, fixation and activation of complement, and chemotaxis of neutrophils and monocytes. The lysis of damaged tissues is carried out by lysosomal enzymes of phagocytes.

Rheumatoid arthritis

Rheumatoid arthritis is a systemic allergic joint disease characterized by proliferation of synovial tissue and erosive-destructive damage to cartilage and ligaments.

Etiology . Currently, the main role in the development of rheumatoid arthritis is assigned to immune complexes. Rheumatoid factor plays an important role in the formation of immune complexes. The rheumatoid factor, according to modern concepts, is class M autoantibodies to the Fc fragment of the host's IgG. The formation of antibodies to their own immunoglobulins is explained by the presence of partial denaturation of the latter.

Contribute to the development of the disease hypothermia, hyperinsolation, intoxication, diseases of the endocrine system, stress. The hereditary predisposition of animals to rheumatoid arthritis has also been established.

Pathogenesis The disease is mainly caused by an allergic reaction of type III. Immune complexes are formed as a result of the binding of rheumatic factor (class M autoantibodies) to class G immunoglobulins of the host.

Rheumatoid factor was found in 20% of affected dogs. Autoantibodies to collagen and cartilage tissue were also found in some animals, which indicates changes in the structure of these tissues.

The reasons for the change in the structure of the body's own tissues have not been precisely established. It is believed that cell damage can be caused by bacteria and viruses. Immune complexes activate complement, the C5 and C3 components of which have a chemotactic effect. It stimulates chemotaxis and lytic activity of phagocytes. Lysosomal enzymes - collagenase, neutral proteinase, as well as interleukin 1 and prostaglandins E1 cause an acute inflammatory reaction of synovial lining cells, their increased division, as well as damage to cartilage and bone tissue.

Clinical picture . Dogs of all ages and all breeds get sick; clinical signs of rheumatoid arthritis usually appear in cold, damp weather, with changes in atmospheric pressure, before rain, after heavy physical exertion, during the period of hormonal changes in the body, after viral and bacterial infections.

They are characterized by a symmetrical lesion at first small, and then large joints. The disease often proceeds slowly with a constant development of the clinical picture, less often it has an acute course. Initially, the joints of the distal parts of the limbs are affected. The disease can occur in the form of mono or polyarthritis.

Articular syndrome is characterized by the presence of stiffness after rest, swelling and soreness of the joints during active movement. There is a general oppression and refusal to feed, with an acute course of an increase in body temperature.

X-ray studies note the presence of periarticular tissue edema, soft tissue infiltration. With erosive polyarthritis, exostoses, ankylosis, dislocations and subluxations are observed.

The detection of rheumatoid factor in blood serum using the Waaler-Rose test is rarely used in veterinary practice due to its low efficiency.

The diagnosis is based on the results of clinical, radiological and laboratory studies.

Rheumatoid polyarthritis must be differentiated from other types of disease that are not associated with immune complexes (infectious arthritis, drug-induced arthritis, etc.)

Treatment rheumatoid arthritis aims to suppress the body's immune response.

Use prednisolone at a dose of 2-4 mg/kg per day until improvement occurs. In the future, the dose of prednisolone is reduced to the minimum effective. In combination with prednisolone, acetylsalicylic acid is prescribed at the rate of 10-20 mg/kg per day.

In severe cases, cytostatic drugs are included in the treatment regimen. Dogs are advised to use the cytostatic cyclophosphamide. Animals weighing up to 10 kg are prescribed cyclophosphamide at a dose of 2.5 mg/kg per day. With a weight of 10-35 kg, the drug is used at the rate of 2.0 mg / kg, with a weight of more than 35 kg - 1.5 mg / kg.

The drug is used 4 days a week for up to 4 months.

With a decrease in the concentration of leukocytes in the blood of a sick animal below 6x109/l, the dose of cyclophosphamide is reduced by 25%, and at a concentration below 4x109/l, the dose is reduced by 50%.

Immunological tolerance

The absence of an immune response to antigenic irritation is called tolerance.

Tolerance to self-tissue antigens is the main mechanism preventing their immune damage.

Violation of the mechanisms of recognition of one's own antigens leads to the development of autoimmune reactions.

Tolerance of the body's immune system in relation to the antigens of vaccine strains of microorganisms is the cause of ineffective immunization.

BIBLIOGRAPHY

1. Denisenko resistance of calves with bronchopneumonia (article). Zh-l Veterinary. 1987. - No. 12. - S. 53-55.

2. Denisenko and nonspecific humoral protection factors in infectious rhinotracheitis and adenovirus infection of calves. (article). Reports of VASKhNIL 1990. - No. 3. - P. 48-51.

3., Smolenskaya - To the question of the correction of the immunodeficiency state of calves. Agricultural biology. - 1992. - No. 6 - S. 122-127.

4., Kruglov immunopathological reactions in the pathogenesis of non-communicable diseases. Materials of the International UM NPK, dedicated to the 85th anniversary of the Academy, Part 6, M .: FGOU VPO MGAVMiB, 2004. - S. 188-190.

5. Immunology. -Moscow “Medicine”, 1989, 367 p.

6. Allergic diseases. -Minsk Belarus, 2000

7. Introduction to veterinary immunology. , 1999

8. Clinical immunology and allergology. G. Lawlor, T. Fisher, D. Adelman - Moscow, 2000

9. Veterinary immunology. W. J. Herbert. - Moscow, 1974, 311 p.

10. Veterinary immunology. , et al., 1982, 304 p.

11. Jones B., Janeway C. A. Jr. Cooperative interaction of B limphocites with antigen-specific helper T-lymphocytes.// Nature.- 1981.-Vol. 292.-P.547-549.

12. McDonald D. M. Lymphocyte receptors // Brit. J. Dermatol Suppl.-1982.-Vol. 107.-No. 23.-P. 69-89.

13. (Paul W. E.) Sex. In 3 volumes. T.1 / Per. from English-M.: Mir, 1987.-360 p.

14. (Canter H) Cantor H. T-lymphocytes // In the book. "Immunology" / Per. from English-M.: Mir, 1987.

15. (Burnet F) Burnet F. Cellular immunology / Per. from English. –M.: Mir, 1971.-537 p.

16. R. Kirk, D. Bonagura. Modern course of veterinary medicine Kirk./ Per. from English. - M.: -Print", 2005. - S. 758-791.

17. J. Simpson, R. Wilse. Diseases of the digestive system of dogs and cats / Per. from English. – M.: -Print”, 2003. – 496 p.

eighteen. , . Diseases of dogs./ Per. from English. - M .: "Aquarium", 2004 - S. 524-577.

Textbook. - M.: Agrovet, 2011. - 752 p.: ill. - ISBN 978-5-905543-01 -2. The book describes in detail the main stages of the formation and development of immunology, incl. in Russia, information about Nobel laureates in immunology is presented. Modern ideas about the structural and functional structure of the immunity of animals, birds and humans are given. The processes of differentiation and functioning of the central cells of the immune system - T- and B-lymphocytes at the organismal, cellular and molecular levels are characterized, functionally different subpopulations of these cells with effector, helper and suppressor activity are described. Modern ideas about antigens and isoantigens (leukocytes, erythrocytes), products of resting and activated cells of the immune system and immunologically significant membrane molecules of these cells (cytokines, immunoglobulins, receptor apparatus, molecules of adhesion, coreception, costimulation, etc.) are given. Various forms and mechanisms of formation of humoral and cellular immunity reactions are presented, including transplantation, mechanisms of tolerance formation (central, peripheral, oral), elimination of "forbidden" clones, etc. The important role of the genetic apparatus of individuals, which controls the maintenance of immunological homeostasis, is shown. Much attention is paid to the histocompatibility complex and its biological functions. The features of innate immunity and the mechanisms of its functioning are described in detail - effector cells (macrophages, natural killers), the mechanisms of recognition of microbial PAMP structures by pattern-recognizing PRR receptors (pathogen molecular mosaic), the role of physical, chemical and humoral factors in the reactions of innate immunity. The role of reactions of innate immunity in the formation of adaptive immunity is shown. ILL-lymphocytes (Innate-like lymphocytes), which play an important role in innate immunity reactions and perform the functions of primary barriers of the immune system — B1-, MzB-, MAIT-, γδT-, and NK-T-lymphocytes, have been characterized.
The textbook is intended for students, graduate students, residents, teachers of veterinary and biological faculties of universities, courses and departments for advanced training of veterinarians and biologists, for scientists, specialists in various fields who are interested in the problems of immunology. Organs and lymphoid tissue of the immune system of animals and birds.
Cells of the immune system: hematopoietic stem cells.
T-lymphocytes.
B-lymphocytes.
Natural killer cells (NK-lymphocytes) and T-lymphocytes with natural killer activity (NKT-lymphocytes).
dendritic cells. Cells of the mononuclear phagocyte system. Granulocytes.
Antigens.
innate immunity.
adaptive immunity. Reactions of the humoral type.
Intracellular signaling pathways and activation of animal and human cells.
Antibodies and their formation in animals and birds.
Major histocompatibility complex and biological significance. Genetic diversity and features of the formation of the antigen-recognizing repertoire of t- and b-lymphocytes.
Cytokines.
Cellular immunity.
immunological tolerance.
Immunological deficiency.
Immunomodulators - drugs for the immune system.
Model systems in immunology.
Immunobiotechnology.

"VETERINARY IMMUNOLOGY Fundamentals Textbook Recommended by the Educational and Methodological Association (UMO) of higher educational institutions of the Russian Federation for education in the field of ..."

V. M. MANKO, D. A. DEVRISHOV

VETERINARY

IMMUNOLOGY

Educational and Methodological Association (UMO)

higher educational institutions of the Russian Federation

on education in the field of zootechnics and veterinary medicine

Publishing house "Agrovet"

UDC 612.083 (075.8)

BBK 28.074ya73

Reviewers:

Fedorov Yuri Nikolaevich,

doctor of biol. Sciences, Professor, Corresponding Member. RAAS, deputy. director of VNITIBP.

Makarov Vladimir Vladimirovich, Doctor of Biol. sciences, professor, head. Department of Veterinary Pathology, PFUR.

Manko V. M., Devrishov D. A.

Veterinary immunology. Fundamentals: Textbook. - K55 M.: Publishing house "Agrovet", 2011. - 752 p.: ill.

ISBN 978-5-905543-01-2 The book describes in detail the main stages of the formation and development of immunology, incl. in Russia, information about Nobel laureates in immunology is presented. Modern ideas about the structural and functional structure of the immunity of animals, birds and humans are given. The processes of differentiation and functioning of the central cells of the immune system - T- and B-lymphocytes at the organismal, cellular and molecular levels are characterized, functionally different subpopulations of these cells with effector, helper and suppressor activity are described. Modern ideas about antigens and isoantigens (leukocytes, erythrocytes), products of resting and activated cells of the immune system and immunologically significant membrane molecules of these cells (cytokines, immunoglobulins, receptor apparatus, molecules of adhesion, coreception, costimulation, etc.) are given.

Various forms and mechanisms of formation of humoral and cellular immunity reactions, including transplantation, mechanisms of tolerance formation (central, peripheral, oral), elimination of "forbidden" immunity are presented.

clones, etc. The important role of the genetic apparatus of individuals, which controls the maintenance of immunological homeostasis, is shown. Much attention is paid to the major histocompatibility complex and its biological functions. The features of innate immunity and the mechanisms of its functioning are described in detail - effector cells (macrophages, natural killers), mechanisms for recognition of PAMP structures of microbes by pattern-recognizing PRR receptors (pathogen molecular mosaic), the significance of physical, chemical and humoral factors in innate immunity reactions. The role of reactions of innate immunity in the formation of adaptive immunity is shown. ILL-lymphocytes (Innate-like lymphocytes), which play an important role in innate immunity reactions and perform the functions of primary barriers of the immune system - B1-, MzB-, MAIT-, T- and NK-T-lymphocytes, are characterized.

–  –  –

All rights reserved. No part of this book may be reproduced in any form without the written permission of the copyright holders.

© V. M. Manko, D. A. Devrishov, 2011 © Agrovet Publishing House, 2011 ISBN 978-5-905543-01-2

Foreword

Conventions

Introduction

Years of insights and discoveries (History of the development of immunology)

Humoral immunity and its factors - antibodies and cytokines

Cellular bases of the humoral immune response.

Subpopulations of lymphocytes and their cooperation. T- and B-lymphocytes

Cellular immunity

Immunological tolerance

Immunogenetics

Stem cells, their quantification and factors controlling progenitor cell functions

Theories of immunity

Allergology

Development of immunology in Russia

Discoveries in the field of immunology, awarded the Nobel Prize ....................................62

Chapter 1. ORGANS AND LYMPHOID TISSUE OF THE IMMUNE SYSTEM

FARM ANIMALS AND BIRDS

Central organs of the immune system

Peripheral organs of the immune system

Organo-circulatory organization of the immune system

1.1. Bone marrow

Hematopoietic cells in the bone marrow

Stromal cells in the bone marrow

Proliferative activity of bone marrow cells

1.2. Thymus (thymus gland)

Thymus and its localization

The structure of the thymus

Thymic lymphocytes, dendritic cells and mononuclear phagocytes

thymus stromal cells

Features of the structure of the thymus of animals and its role in immunity

1.3. Fabricius' bag of birds

Functions of the Bag of Fabricius

The structure of the Bag of Fabricius

1.4. Lymph nodes of animals and features of their structure

Functions of the lymph nodes

The structure of the lymph node

Localization of T- and B-lymphocytes in the lymph node

1.5. Hemolymph nodes

1.6. Spleen

Functions of the spleen

The structure of the spleen

Localization in the spleen of cells of the immune system and its features in different species of animals and birds

1.7. Liver

1.8. Lymphoid tissue of mucous membranes and skin

1.8.1. Lymphoid tissue of the skin

1.8.2. Lymphoid tissue of the respiratory tract

1.8.3. Lymphoid tissue of the gastrointestinal tract

1.8.3.1. tonsils

1.8.3.2. Big omentum

1.8.3.3. Group lymphatic follicles (Peyer's patches) and features of their structure in different animal species

Structured lymphoid tissue of Peyer's patches

Diffuse lymphoid tissue of Peyer's patches

1.8.3.4. Appendix

1.9. Abdomen

1.10. Blood and lymph

Chapter 2

CELLS

2.1. Cell populations of the immune system

2.2. stem hematopoietic cells

Pluripotent stem cells

multipotent stem cells

Lineage-specific stem cells at early stages of embryogenesis.......108 Stromal stem cells

2.2.1. Stem hematopoietic cells and their localization in the bone marrow..........108 2.2.2. Hematopoietic stem cell differentiation

2.2.3. Plasticity of hematopoietic stem cells

2.2.4. Stem cell cultivation

2.2.5. Hormonal and thymic control of hematopoietic stem cell migration

2.2.6. Lymphocyte control of proliferation and differentiation of hematopoietic stem cells

Chapter 3. T-LYMPHOCYTES

3.1. Bone marrow progenitors of T-lymphocytes

3.2. Intrathymic progenitors of T-lymphocytes

3.3. Antigen recognition complex of T-lymphocytes TCR-CD3

3.3.1. Membrane complex TCR

3.3.1.1. Hypervariable and framework regions of TCR

3.3.1.2. -Homodimer of the TCR complex

3.3.2. CD3 complex

3.3.3. CD4 and CD8 co-receptors

3.4. Subpopulations of T-lymphocytes of animals and humans

3.4.1. T-lymphocytes

3.4.2. T-lymphocytes

3.4.3. Cytotoxic T-lymphocytes (T-killers)

3.4.4. Regulatory T-lymphocytes

3.4.4.1. T-helpers (Th)

3.4.4.2. T regulatory cells (TReg)

T-lymphocytes of CD4 phenotype

T-lymphocytes of the CD4+CD25+ phenotype

T-lymphocytes of the CD8+CD28– phenotype

Veto cells

MAIT lymphocytes

3.4.4.3. T-differentiating lymphocytes (Td)

3.4.5. Memory T cells (Tm)

Chapter 4. B-LYMPHOCYTES

4.1. Stages of differentiation of B-lymphocytes in the bone marrow

4.2. Antigen recognition receptor of B-lymphocytes

4.3. Subpopulation organization of the B-system of animal and human lymphocytes ..........155 4.3.1. B-effectors

4.3.1.1. B1-lymphocytes (B1)

4.3.1.2. B-lymphocytes of the marginal zone (MzB - Marginal zone B cells)

4.3.1.3. B2 lymphocytes (B2)

4.3.2. Helper B cells

4.3.3. B-suppressors (Suppressor B cells)

4.3.4. Memory B cells

Chapter 5. NATURAL KILLER CELLS (NK-LYMPHOCYTES) AND

T-LYMPHOCYTES WITH NATURAL KILLER ACTIVITY

(NKT-LYMPHOCYTES)

5.1. Natural killer cells (NK-lymphocytes)

5.2. T lymphocytes with natural killer activity (NKT cells)

5.3. Cells of various histological types with cytolytic activity..........177

Chapter 6. Dendritic cells. CELLS OF THE MONONUCLEAR SYSTEM

PHAGOCYTES. GRANULOCITES

6.1. Dendritic cells

6.1.1. Langerhans cells

6.1.2. interstitial dendritic cells

6.1.3. Lymphoid or thymic (interdigital) dendritic cells

6.1.4. Follicular dendritic cells

6.2. Cells of the mononuclear phagocyte system

6.2.1. Monocytes

6.2.2. macrophages

6.3. Granulocytes

6.3.1. Neutrophil granulocytes (neutrophils)

6.3.2. Eosinophilic granulocytes (eosinophils)

6.3.3. Basophilic granulocytes (basophils)

6.4. mast cells

6.5. platelets

6.6. endothelial cells

Chapter 7. ANTIGENS

7.1. Antigens and conditions that determine their immunogenicity

7.2. Microbial antigens

7.3. Superantigens

7.4. RBC antigens

7.4.1. Isoantigens of erythrocytes of blood groups A, B, 0

7.4.1.1. Genetic control of expression of isoantigens of blood groups A, B, 0

7.4.1.2. Subgroups of isoantigens of the A, B, 0 system

7.4.1.3. The nature and structure of isoantigens of the A, B, 0 system

7.4.1.4. Expression of erythrocyte isoantigens on cells, tissues and secretions

7.4.1.5. Induction of an immune response to isoantigens A, B, 0. Laws of blood transfusion

7.4.1.6. Isoantigens of erythrocytes of blood groups A, B, 0 and diseases

7.4.2. Isoantigens of erythrocytes of the Rhesus system

7.4.2.1. The nature of the antigens of the Rhesus system

7.4.2.2. Antibodies to antigens of the Rhesus system and neonatal erythroblastosis....236 7.4.2.3. Diagnosis and prevention of hemolytic disease

7.4.3. Isoantigens of erythrocytes of domestic animals

7.4.3.1. Features of erythrocyte isoantigens of animals

7.4.3.2. Incompatibility reactions that develop in animals during the interaction of antibodies with erythrocyte isoantigens

7.5. Leukocyte antigens

7.5.1. Antigens (MHC) of human leukocytes

7.5.2. Antigens (MHC) of domestic animal leukocytes

Chapter 8

8.1. Features of innate immunity

Emigration of leukocytes from a blood vessel into tissues (diapedesis)

8.2. Factors of innate immunity of animals and humans

8.2.1. Physical factors

8.2.2. Chemical Factors

8.2.3. Cellular factors

8.2.3.1. Phagocytes and endocytosis reactions

8.2.3.2. Extracellular degranulation - exocytosis

8.2.3.3. Cytolytic action of NK cells

8.2.4. Humoral factors

8.2.4.1. Complement system

8.2.4.2. Perforin-granzyme cytotoxins

8.2.4.3. Antibiotic peptides

8.2.4.4. Acute phase proteins

8.2.4.5. Other humoral factors of pre-immune inflammation

Chapter 9. ADAPTIVE IMMUNITY.

REACTIONS OF THE HUMORAL TYPE ......... 289

9.1. Adaptive immunity and its forms

9.2. Humoral immunity and features of its formation in animals and humans

9.2.1. Latent phase of the immune response

9.2.1.1. Cell interaction. Three cell immunogenesis system

9.2.1.2. Mechanisms of Cell Interaction in Humoral Immunity Reactions...297 Adhesion Molecules

Formation of antigenic peptide–product of major histocompatibility complex class II genes

Double recognition effect

APC-T-helper interaction and mechanisms of antigen recognition

T-helper-B-lymphocyte interaction and the formation of an antibody-synthesizing mechanism

9.3. Formation of antibodies to T-independent antigens

9.4. Formation of the immune response to the hapten-carrier conjugate

9.5. The role of the components of the skin immunity system in the formation of the immune response

9.6. The role of the components of the immune system in the formation of the immune response in the mucous membranes

9.6.1. Components of the immune system that form the immune response in the mucous membranes of the gastrointestinal tract

9.6.2. Components of the immune system that form the immune response in the mucous membranes of the respiratory and genitourinary tracts 324 Chapter 10. INTRACELLULAR SIGNALING PATHWAYS AND ACTIVATION OF ANIMAL AND HUMAN CELLS

10.1. Formation of signaling pathways that activate the functional activity of cells of the immune system

10.1.1. Intracellular signaling pathways activating B-lymphocytes .................................329 10.1.2. Intracellular signaling pathways that activate T-lymphocytes

10.1.3. Intracellular signaling pathways that activate natural killer cells (NK-lymphocytes)

10.1.4. Formation of phagocyte signaling pathways mediated through the activation of PRR receptors

10.1.5. Formation of signaling pathways mediated through the activation of receptors for cytokines

10.2. Formation of signaling pathways that suppress the functional activity of cells of the immune system

10.3. Apoptosis (programmed cell death)

10.3.1. Receptor mechanism of apoptosis induction

10.3.2. Mitochondrial mechanism of apoptosis induction

10.3.3. Cell death induced by their activation

Chapter 11. ANTIBODIES AND THEIR FORMATION IN ANIMALS AND BIRDS

11.1. Logarithmic (exponential) phase of antibody production

11.2. Cooperation of cells at the level of mature antibody producers

11.3. The structure of immunoglobulins (antibodies)

11.4. Properties of immunoglobulins (antibodies)

Normal antibodies

Immunoglobulin superfamily

Monoclonal antibodies

11.5. Regulatory role of immunoglobulins in antibody production

11.6. Genetic control of antibody production

11.7. Antigen–antibody interaction

Chapter 12

BIOLOGICAL SIGNIFICANCE.

GENETIC DIVERSITY

AND FEATURES OF THE FORMATION OF ANTIGEN RECOGNIZING

REPERTOIRE OF T AND B LYMPHOCYTES

12.1. Major histocompatibility complex and its biological significance..........411 12.1.1. Major histocompatibility complex - history of discovery, structure........412 12.1.2. Major histocompatibility complex of domestic animals and birds......417 12.1.3. The concepts of “genotype”, “haplotype”, “phenotype”

12.1.4. Double recognition effect

12.1.5. Genetic control of the immune response

12.1.6. The role of the major histocompatibility complex in the quality control of the immune response. Relationship between human major histocompatibility complex and disease resistance and susceptibility 422 12.1.7. Association of the major histocompatibility complex of domestic animals with resistance and susceptibility to diseases .................................................426 12.1.8. Major histocompatibility complex and reproduction

12.2. Genetic diversity of antigen-recognizing structures of immunoglobulins, receptors of T- and B-lymphocytes and features of its formation

12.2.1. Structural organization of the germline genes of the antigen-recognizing T-lymphocyte receptor (TCR)

12.2.2. Structural organization of germline genes for light (Ig and Ig) and heavy (IgH) immunoglobulin chains

12.2.3. Structural organization of the recombinant signal sequence

12.2.4. Mechanism of V(D)J recombination

Chapter 13. CYTOKINES

13.1. The main stages of the study of cytokines

13.2. Cytokines and hormones

13.3. Areas of action of cytokines

13.4. Features of the action of cytokines

13.5. Classification of cytokines

Classification of cytokines by function

Classification of cytokines by structure

Receptors for cytokines

13.6. The most significant cytokines and their functions

Interleukins (IL)

Interferons (INF)

Type I interferon family (INF-I)

Tumor necrosis factor (TNF) and its superfamily

Transforming growth factor (TGF) and its family

Colony-stimulating factors and regulation of hematopoietic progenitor functions

Chemokines

Chapter 14

14.2. Reactions of cellular (transplantation) immunity against transplanted genetically alien cells, tissues, organs

14.3. Genetic laws of tissue compatibility

14.4. Immunological nature of rejection of a genetically alien transplant

14.5. Significance of T- and B-lymphocytes in reactions of cellular incompatibility ............... 502

14.6. Direct and indirect antigen presentation by antigen-presenting cells to T-lymphocytes

14.7. Adoptive transfer of immunity

Chapter 15. IMMUNOLOGICAL TOLERANCE

15.1. Discovery of tolerance

15.2. Induction of tolerance to exogenously introduced antigens

15.2.1. adaptive period. Tolerance induction in adulthood

15.2.2. Antigen and its form. Low-dose and high-dose tolerance ...... 522 15.2.3. Features of the induction of immunological tolerance

15.3. Oral tolerance

15.4. Induction of tolerance to self-antigens. Central and peripheral tolerance

15.5. Immunologically Preferential Territories and Tolerance .................................529 Chapter 16. IMMUNOLOGICAL DEFICIENCY

16.1. Congenital (primary) immunodeficiencies

Combined deficiency of T- and B-links of immunity

Primary insufficiency of the B-cell link of immunity .............................552 Predominant insufficiency of the T-cell link of immunity ..................554 Birth defects of the phagocytic system

Birth defects of the complement system

16.2. Acquired (secondary) immunodeficiencies

16.3. Diagnosis of immunodeficiency states

Chapter 17. IMMUNOMODULATORS - DRUGS FOR THE IMMUNE SYSTEM

17.1. Classification of immunomodulators

17.2. Adjuvants

17.3. Immunosuppressants

17.4. Immunostimulants

17.5. Individual susceptibility to the action of immunomodulators .................614 Chapter 18. MODEL SYSTEMS IN IMMUNOLOGY

18.1. Model systems at the organism level

18.1.1. line animals

Model system for determining the processes of proliferation and differentiation of endogenous stem hematopoietic cells in the spleen of mice

Model system for determining the number of antibody-forming cells and their precursors in the spleen of mice

Cunningham's modification (A.J. Cunningham, 1965) of determining the number of antibody producers

Model system for the induction of delayed-type hypersensitivity (DTH) and its severity in mice

18.1.2. Germ-free animals

18.2. Model systems based on the in vivo cell culture method

18.2.1. Model systems for studying in vivo culture the mechanisms of humoral and cellular immunity, cellular interactions and patterns of functioning of hematopoietic stem cells, T- and B-lymphocytes

18.2.2. Model systems for studying in vivo culture the activity of biological, physical or chemical factors

18.3. Model systems based on the in vitro cell culture method

Chapter 19. IMMUNOBIOTECHNOLOGY

Prophylactic anti-infective drugs (vaccines) of a new generation created by methods of immunobiotechnology

Obtaining monoclonal, bispecific and chimeric antibodies by methods of immunobiotechnology (G. Khler, C. Milstein, 1975)

Creation of immunotoxins by immunobiotechnological methods

Immunobiotechnology and development of immunomodulatory drugs

APPS

Appendix I. Human CD (Cluster of Differentiation) marker antigen system

Annex II. Bovine CD antigens

Annex III. Equine CD antigens

Annex IV. Terminological dictionary

FOREWORD

Textbook “Veterinary Immunology. Fundamental Foundations” was written by a well-known immunologist and immunogeneticist, Academician of the International Academy of Sciences of Ecology and Life Safety, Professor V.M.

Manko and Honored Veterinary Doctor of Russia, Corresponding Member of the Russian Academy of Agricultural Sciences Professor D.A. Devrishov. The release of the textbook is event-driven. This eventfulness is determined by a number of facts.

In recent years, there has been an increasing demand for immunology in veterinary universities. One example of this is the organization in 2003 of the country's first department of veterinary immunology at the Moscow State Academy of Veterinary Medicine and Biotechnology. K.I.

Scriabin, which produces a large detachment of specialists, incl. and in the field of immunology. Against this background, the absence of a textbook on veterinary immunology is quite noticeable, in connection with which the student audience is forced to use textbooks and / or teaching aids not on veterinary medicine, but on medical immunology. That is why the publication of a textbook for veterinarians of various profiles is a significant event, at least to a small extent filling the vacuum that has formed.

It should be noted that veterinary immunology has not yet reached the depths in the knowledge of the mechanisms of immunity, which are currently characterized by medical immunology, which is also associated with the diversity of animal species. However, the authors have done a great job of describing the features of the immunological reactivity of page - x. and pets. When characterizing the regularities of the functioning of the immune system, the authors often refer to the regularities established for the human population. In general, this is justified, since the mechanisms of immunity in mammals are similar, and this made it possible to describe all the main phenomena of immunity and the patterns of functioning of the immune system, its effector functions and regulatory activity at the molecular genetic, cellular and organismal levels. This approach makes the textbook useful not only for veterinarians, but also for general biologists, as well as for medical workers interested in veterinary and general biological problems of the immunological discipline.

Moreover, problems already solved by veterinary immunologists and problems that have yet to be explored become apparent. And this is another important reason that determines the significance of the publication of the textbook.

Finally, the originality of the construction of the material is essential.

Each of the chapters not only reflects in a concise form almost all the basic information on this topic, but is also provided with a background in solving this problem.

FOREWORD

Problems. Interesting and important for understanding the history of the development of immunological ideas is the chapter devoted to the description of the formation and development of immunology from ancient times to the present day. In general, the authors succeeded in presenting all the main sections of modern fundamental immunology in a rather concentrated form in a clear and good language.

The textbook is original in its style of presentation, very useful for students, residents, graduate students, teachers of veterinary medicine, for a wide range of veterinarians, as well as for biologists and specialists from other disciplines interested in the problems of immunological science.

Academician of RAS, RAMS and RAAS R.V. Petrov, Academician of the Russian Academy of Agricultural Sciences E.S. Voronin

SYMBOLS

AG - antigen;

AMP - adenosine monophosphate;

APC - antigen-presenting cell;

AT - antibody;

HIV - human immunodeficiency virus;

BCR - B-cell receptor;

MHC - major histocompatibility complex;

G-CSF - granulocyte colony-stimulating factor;

GM-CSF - granulocyte-macrophage colony-stimulating factor;

GIT - gastrointestinal tract;

IL - interleukin;

INF - interferon;

kD - kilodalton;

CSF - colony stimulating factor;

LPS - lipopolysaccharide;

mAb - monoclonal antibody;

M-CSF - macrophage colony-stimulating factor;

GVHD - graft-versus-host disease;

TKR - T-cell receptor;

TNF - tumor necrosis factor;

HLA (Human leucocyte antigen) - human leukocyte antigen;

Ig - immunoglobulin;

ITAM (Immunoreceptor tirozine-based activation motiv)) - tyrosine-containing activation sequences of amino acids in immunoreceptors;

ITIM (Immunoreceptor tirozine-bazed inhibit motiv) - tyrosine-containing inhibitory amino acid sequences in immunoreceptors;

MHC (Major histocompatibility complex) - major histocompatibility complex; MHC-I, MHC-II - major histocompatibility complex classes I and II, respectively;

NK (Natural killers) - natural killer cells;

NK-T cells - T-lymphocytes with natural killer activity;

Th - T-helpers;

Th0 - T-helper precursors;

Th1 - type I T-helpers (regulate cellular immune responses);

Th2 - type II T-helpers (regulate humoral immunity responses).

INTRODUCTION

Immunology is characterized by a high level of development from the first years of its formation to the present day. Success in the development of its problems has been marked by a large number of Nobel Prizes (see the chapter "Years of Insights and Discoveries"). Immunology has entered clinical practice. Observations of leading domestic and foreign clinical centers have shown that there are no diseases that are not induced by disorders in the immune system or diseases that do not lead to its disorders, resulting in their significantly more severe, prolonged and complicated course. To diagnose immunopathologies, detect disorders in the immune system, monitor the therapy used, and mass assess the immune status in order to detect immunodeficiencies and predict their possible development, panels of monoclonal antibodies have been created, which play an outstanding role in the development of fundamental problems of immunology. New immunodiagnosticums, immunotropic, immunomodulatory drugs, adjuvants and vaccine preparations have been developed and are being created, new methods of immunotherapy of diseases are being developed. The demands of clinical practice have been a powerful stimulus for the further development of fundamental immunology. The demand for immunology in clinical medical practice, in fundamental and applied research is widely reflected in the creation of departments of immunology, courses and departments for advanced training of allergologists-immunologists in many universities of the country. A huge number of textbooks, various teaching aids and monographs on medical immunology have been published both abroad and in Russia, many of which have become desktop. So, for example, in addition to the well-known textbooks on immunology, V.I. Ioffe (1968), A.E. Vershigory (1975, 1980), R.V. Petrova (1982, 1987), A.Ya. Kulberg (1985), V.G. Galaktionova (1998, 2000, 2004), A.A. Yarilina (1999, 2010), A.V. Karaulova et al. (1999, 2005), G.N. Drannik (1999, 2003, 2006), R.M. Khaitova et al. (2000, 2002, 2010), N.N. Popova et al.

(2004), R.M. Khaitov (2006, 2008, 2010) and others are known three-volume books on immunology (edited by W. Paul, 1987–1989) and on clinical immunology and allergology (edited by L. Yeager, 1990), a guide to clinical immunology and allergology ( under the editorship of G. Lolor, Jr. et al., 2000). For a number of years, a translated textbook on immunology by I. Royt et al. has been published in Russia.

In 2007–2008 manuals on visual immunology (G.-R. Burmester et al.) and on visual allergology (M. Röken et al.) were published in 2003 and 2008. - atlas of medical microbiology, virology and immunology (under the editorship of A.S. Bykov, A.A. Vorobyov and V.V. Zverev), in 2010 R.M. Khatov, A.A. Yarilin and B.B. Pinegin published an atlas on immunology, etc.

14 INTRODUCTION

Despite great progress in the field of veterinary medicine, the achievements of immunology in this area are less tangible. The first department of veterinary immunology in the country was established at the Moscow State Academy of Veterinary Medicine and Biotechnology named after M.V. K.I. Scriabin only in 2003. There are practically no textbooks on modern veterinary immunology. Previously created textbooks on veterinary immunology (P.M. Outteridge, 1985; Ya.E. Kolyakov, 1986; Voronin E.S. et al., 2002) are actually outdated or do not fully reflect the achievements of modern immunological science. Modern textbooks on veterinary immunology are numbered in units (I.R. Tizard, 2009) and are not widely available. Meanwhile, in recent years, new data have appeared that significantly deepen our understanding of the structure and functions of the animal immune system, which is highly significant for clinical practice. Given the great interest of the student audience, graduate students and veterinarians in the problems of immunology, we decided to do hard work - at least to a small extent to fill the resulting vacuum. The first part of the textbook “Veterinary immunology. Fundamental Foundations” considers the central problems of immunological science - the structure and functions of the immune system. This part of the textbook contains 20 chapters, which characterize the main milestones in the formation and development of immunology and allergology, describe the structural and functional structure of the immune system.

Concepts are given about functionally different cell systems, populations and subpopulations of T- and B-systems of immunity, which ensure the maintenance of genetic homeostasis of animals in response to the intake of various forms of antigen into the body, about the mechanisms of formation of immunological reactions of innate and adaptive immunity, central, peripheral and oral tolerance. . Particular attention is paid to the description of the central effectors of innate immunity (macrophages, natural killers), non-classical forms of lymphocytic subpopulations (B1-, MzB-, MAIT-, T and NK-T-lymphocytes) and pattern recognition receptors (PRR) that recognize the molecular mosaic of pathogens (PAMP- ligands), which provide the basis for the formation of adaptive immunity reactions and are the first line of antimicrobial defense of the body. Ideas about myeloid cells involved in immune responses are given. The molecular mechanisms of the formation of the antigen-recognizing receptor apparatus of lymphocytes, cellular interactions and signaling pathways leading to the activation of cells of the immune system are described. Soluble products of immunocytes (cytokines, antibodies, antibiotic peptides, complement system, etc.) through which the functions of effector cells are mediated are described and characterized. Modern ideas about the genetic mechanisms of control of the induction and development of immune responses, about the main histocompatibility complex in humans and animals and its biological functions are given. Primary and secondary immunodeficiencies in animals and immunomodulators used to normalize acquired immune disorders are described.

INTRODUCTION

Information about the achievements of immuno- and nanobiotechnology is also given. Model systems used for research purposes in the field of immunology are described. The appendices contain descriptions of human and animal CD systems, a terminological dictionary, and recommended reading.

Thus, a huge contingent of students, residents, graduate students, teachers of not only veterinary universities, but also biological, veterinary doctors and researchers in the field of veterinary medicine receive the latest information on modern immunology, described in the textbook based on the revealed facts and patterns formulated on their basis. . All comments and suggestions will be accepted by the authors with gratitude.

biol. Sciences T.P. Zharovoy, Ph.D. biol. Sciences G.N. Pechnikova, Ph.D. vet. Sciences V.E. Brylina, as well as Dr. Vet. sciences, prof. P.A. Emelianenko for the constant support and help, especially during the preparation of the textbook for publication.

V.M. Manko, D.A. Devrishov 25.02.2010

YEARS OF INSIGHTS AND DISCOVERIES

(HISTORY OF THE DEVELOPMENT OF IMMUNOLOGY)

Modern immunology, like many other disciplines that make up the history of the development of Life Sciences, has its roots in the distant past.

However, not many of them have such an impressive list of insights and discoveries awarded the highest award of the scientific community - the Nobel Prize (see table). This discipline is the subject of research by many brilliant minds who have made a significant contribution to the development of immunology, thanks to the insights and discoveries of which the already created ones are polished and new facets of knowledge in immunology and related disciplines - physiology, cytology, microbiology, biochemistry, biotechnology and many others are opened.

And, finally, immunology itself is one of the few that have made a huge contribution to practical health care and agriculture due to the constantly accumulating, updating and deepening knowledge in the field of fundamental research and the implementation of their results in practice. Immunology has made an invaluable contribution to the development of prevention, diagnosis and therapy of many infectious and somatic diseases in humans and animals, their rehabilitation and disease prognosis. Despite more than two centuries of development history, immunology is a surprisingly young discipline, intensively developing in a huge number of "hot spots" up to the present day.

The first information from the field of immunology came to us from time immemorial, incl. from the Ancient East, Ancient Greece, Rome, Egypt and were associated with the description by historians of raging epidemics of such terrible devastating diseases as plague, smallpox, cholera. The most important observation of those early years was the conclusion about the resistance of recovered and surviving people to re-infection. This allowed the sick to care for the sick and bury the dead. Subsequently, resistance to re-infection began to be called immunity (from "immunitas"), which in ancient Rome meant the release of a citizen from service or any other public service.

Of the well-known healers of later years, history has preserved for us a number of names who have made an important contribution to the development of immunological knowledge. Thus, the Persian physician, philosopher and alchemist Rhazes (865–932) - Rhazes (Abu Bakr Muhammad ibn Zakarija) believed that smallpox, which mainly affects young men, is due to an excess of moisture in the blood, which, as a result of fermentation, pours out through the pustules formed during smallpox. The absence of excess moisture leads to long-term immunity to the disease, since

YEARS OF INSIGHTS AND DISCOVERIES

there is no substrate necessary for infection. The thing is that a person in the process of life (from birth to old age) is constantly approaching dryness. In this regard, the blood of infants and children is much more moist than the blood of young men and, especially, old people. It is because of the humidity of the blood that young men mainly fall ill, but not the elderly. Rhazes not only clearly differentiated smallpox from measles and other infectious diseases, but also tried to treat people bitten by scorpions with the serum of donkeys who had been ill after being bitten by these arthropods.

Observations regarding resistance to re-infection with smallpox substantiated the possibility of variolation (smallpox inoculation) using the crust or contents of the pustules of patients with a "favorable" course of the disease, administered to healthy individuals to prevent possible infection. Variolation techniques were especially developed in China, where pustule materials were blown into the nostril (for boys - on the left, for girls - on the right) or applied to skin incisions.

The concept of one or another substrate present in the body and providing the possibility of infection by a pathogen, and about the depletion of this substrate, leading to recovery, has been common among many researchers of the human body for a long period of time.

Thus, the Italian physician Girolamo Fracastoro (Girolamo Fracastoro) believed that the disease is caused by small seeds (contagia) that have an affinity for a particular plant, animal or person and can be transmitted from one organism to another over long distances through clothing or household items. In the body, contagia have an affinity for a particular organ or body fluid, where they create other seeds similar to themselves. Thus, smallpox has an affinity for the admixture of menstrual blood, which reaches the embryos of mammals in utero. When infected, the remnants of menstrual blood begin to ferment, protrude to the surface of the skin in the form of pustules and are excreted when the pustules burst, cleansing the body of these impurities. With the admixture of menstrual blood, all organisms are born; without it, the disease cannot resume. In other words, the release of the body from the remnants of menstrual blood leads to the development of acquired immunity. In the same way, the body acquires immunity to other infectious diseases. Fracastoro outlined these views in his work “On contagion, contagious diseases and treatment”, published by him in Venice in 1546.

Frakostoro's ideas were subjected to significant criticism by Heironymus Mercurialis. The latter believed that if Fracostoro was right, getting rid of the remnants of menstrual blood during smallpox should have led to the immunity of the body to measles. Such "cross-immunity", according to Mercurialis, is contrary to the facts.

Apparently, the ideas of Fracastoro and Mercurial are the first attempts to explain the nature of natural immunity to diseases, their specificity and contagiousness.

HISTORY OF THE DEVELOPMENT OF IMMUNOLOGY

In general, thanks to the analysis of observations on diseases and attempts to treat them, by the middle - end of the 16th century it became obvious that:

individuals who have recovered from an infectious disease become immune to re-infection with the same pathogen, they develop a state of immunity to it;

an infectious disease can be transmitted at a distance from one individual to another with the help of self-reproducing infectious factors - "seeds" or "embryos" (seminaria);

recovery from an infectious disease is not an obstacle to contracting another infection, i.e. characterized by specificity.

One of the most important postulates was that sensitivity to infection with pathogens was determined, as it was believed, by the presence in the body of a certain substrate sensitive to the action of microbes, while its absence characterized resistance to the disease. In principle, the great Pasteur, the founder of immunology, adhered to this point of view, believing that specific substances are necessary for the reproduction of native microbes or their attenuated strains.

When they are depleted, microbial growth stops. The state of acquired immunity lasts only as long as these unique substances are not formed again. Studies of subsequent years (Theobald Smith, Shibasaburo Kitazato, Emil Behring and others) demonstrated that the state of immunity can be achieved not only with the help of live microbes, but also killed ones, as well as with the help of the supernatant of broth cultures. Thus, the inconsistency of the prevailing point of view was proved, incl. and Pasteur's point of view. However, as it turned out, this objection is valid only when applied to the creation of acquired immunity. Innate immunity to certain infections is interpreted today from the standpoint of the absence of certain factors that contribute to the reproduction of the pathogen, or, conversely, the presence of factors that block its survival. In any case, the presence or absence of such factors is under the genetic control of a particular individual.

At the beginning of the 18th century, variation spread widely in Europe. Lady Mary Wortley Montagu (1689-1762) - the wife of the English ambassador to Turkey (1716-1718) contributed to this to a large extent.

In 1717, her 6-year-old son was vaccinated against smallpox in Constantinople, and then in England in 1721, her 4-year-old daughter. In 1722, in England, thanks to the efforts of Lady Montagu, smallpox vaccination was introduced as a means of preventing smallpox. To a significant extent, this was facilitated by smallpox vaccination of members of the royal family.

In 1746, voluntary vaccinations against smallpox were introduced in London, and in 1756 smallpox vaccination began in Russia. In 1768, Empress Catherine II and her son Paul I were vaccinated against smallpox.

–  –  –

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Several important animal models (in vivo) have been developed that have experimental value and clinical utility and are comparable to the in vitro systems mentioned earlier. Inbred lines of mice with different genetic profiles were used as models; some of them were obtained by genetic engineering. Animals of some inbred lines have an innate predisposition to the development of certain diseases (eg, breast cancer, leukemia, autoimmune diseases, severe combined immunodeficiency).

In addition, animals with genetic disorders capable of expressing some cloned foreign genes (the so-called transgenic mice), or animals in which the given genes are not expressed (mice with "knockout" genes) have been bred. Such lines are used to study the consequences of the expression of certain transgenes or the consequences of the absence of gene expression in "knockout" mice. Let's start the discussion with animal inbred lines.

Inbred lines

Many classical experiments in the field of immunology have been carried out using inbred animal lines such as mice, rats and guinea pigs. The formation of an inbred line usually results in selective inbreeding of offspring for more than 20 generations. All members of an inbred line of animals are genetically identical. Therefore, they are called syngenes, like identical twins. The immune response of an inbred line can be studied without taking into account the variability associated with genetic differences between animals.

Organ transplantation between members of an inbred line is always successful because their major histocompatibility complex (MHC) antigens are identical. Indeed, knowledge of the laws of transplantation and the fact that the MHC is a major genetic barrier to transplantation came from experiments on inbred lines.

Experiments using inbred lines led to the identification of MHC class I and II genes, the main function of which is the delivery of antigen peptide fragments to the cell surface, which allows epitopes to be recognized by antigen-specific T-lymphocytes.

Adoptive transfer and passive immunization

Protection against many diseases is provided by cell-mediated immunity provided by antigen-specific T cells, as opposed to antibody-mediated (humoral) immunity. The difference between these two branches of the immune system is well demonstrated by adoptive (borrowed) transfer of T cells or passive administration of antisera or purified antibodies.

Adoptive transfer of T cells is usually carried out in genetically identical donor-recipient pairs (for example, within an inbred line) and results in the formation of long-term adoptive immunity after the first contact with the antigen. On the contrary, passive transfer of serum containing antibodies can be carried out without taking into account MHC barriers and remains effective only for as long as the transferred antibodies remain active in the recipient. That is why this type of transfer is called passive immunization.

Mice with severe combined immunodeficiency

Severe combined immunodeficiency (SCID) is a disorder in which the maturation of B and T cells is disrupted, leading to the development of an insufficiency in the mechanisms of lymphocytic defense in an individual. In 1980, an inbred line of mice was bred that spontaneously developed an autosomal recessive mutation leading to SCID. Due to the lack of functioning T and B cells in SCID mice, cell and tissue grafts from mice of other strains or species have engrafted. Such SCID mice can be injected with human hematopoietic stem cells to create human SCID chimeras.

These chimeric mice develop mature functional T and B cells that are the progeny of the injected human hematopoietic stem progenitor cells. This animal model has become a valuable research tool because it allows immunologists to manipulate the human immune system in vivo and explore the development of different lymphoid cells. What's more, human SCID mice could be used to test emerging vaccines, including those that could help protect humans from HIV infection.

Thymectomized and Nude Mice

The importance of the thymus in the development of mature T cells can be demonstrated in mice that underwent thymectomy, irradiation, and then syngeneic bone marrow transplantation during the neonatal period. These mice do not develop mature T-lymphocytes. Also, mice homozygous for the recessive pi/pi mutation do not develop mature T cells because the mutation results in a phenotype characterized by the absence of thymus and hair (hence the term "nude" - naked). In both situations, T cell development can be restored by transplanting thymic epithelial tissue into these mice. Like the SCID mouse models, these animal models are useful in studying T-lymphocyte development. They have also been used to propagate in vivo tumor cell lines and fresh tumor explants from animals of other strains or species, which require the absence of T cells to reject such foreign cells.

Transgenic mice and gene manipulation

Transgenic mice

Another important animal model actively used in immunological research is the transgenic mouse. They are obtained by introducing a cloned gene (transgene) into a fertilized mouse egg. The eggs are then injected into the pseudo-pregnant mouse (Figure 5.14). The success rate of this technique is relatively low, with 10-30% of progeny expressing the transgene. Since the transgene is introduced into both somatic and germ cells, it is transmitted to offspring as a Mendelian trait.

Rice. 5.14. General procedure for obtaining transgenic mice

By constructing a transgene with a given promoter, gene expression can be controlled. For example, some promoters only work in certain tissues (in particular, the insulin promoter only works in the pancreas). Other promoters are activated in response to biochemical signals, which in some cases can be introduced as a dietary supplement (for example, the metallothioneine promoter is activated in response to zinc, which can be added to drinking water). Transgenic mice have been used to study genes that are not normally expressed in vivo (eg, oncogenes).

The action of individual immunoglobulin molecules, T-cell receptors, MHC class I and II molecules, and cytokines was also studied with the help of transgenes. Transgenic mice have been bred in which the entire mouse immunoglobulin locus has been replaced by human immunoglobulin genes. This model is used to generate "human" antibodies in mice. It should be noted that the disadvantage of the transgenic method is that the transgene is inserted into the genome randomly. This limitation, together with the fact that transgene expression in large quantities in different tissues is not physiological, obliges researchers to interpret the results obtained in transgenic mice very carefully.

Mice with "knockout" genes

Sometimes it is interesting to determine how the removal of a particular gene product will affect the immune system. Using the method of gene manipulation, it is possible to replace a normal gene with a mutated or damaged one, creating a mouse with a “knockout” (“knocked out”) gene. Thus, unlike the method used to create transgenic mice, with this method, knockout mice express transgenes inserted into their own specific genes through a process called homologous recombination.

Hypothetically, any gene for which a mutated or damaged transgene exists could be replaced in this way. Knockout mice have been bred that lack the expression of various important genes, including those encoding certain cytokines and MHC molecules. "Knockout" mice were used to identify regions of the gene necessary for its normal functioning. To do this, various mutant gene copies were introduced back into the genome by transgenesis, which led (or did not lead) to the restoration of the functioning of the gene.

Gene Expression Analysis

Microarrays in the Study of Gene Expression

Microarrays, or gene chips, are powerful tools for studying the level of expression of thousands of genes simultaneously. A microarray is made up of thousands of DNA fragments (each with a unique sequence) attached in a specific order to glass or another surface. These DNA fragments in the form of complementary DNA (cDNA; approximately 500-5000 base pairs) or oligonucleotides (20-80 base pairs) can represent genes from all parts of the genome. In this case, it is possible to prepare specialized microarrays that will use only the DNA of the studied genes. The study uses a sample of common messenger RNA (mRNA) - a product resulting from the transcription of all active genes.

For microarray studies, a sample of total mRNA from a cell or tissue is usually tested in parallel with a control sample needed to compare gene expression. For example, different types of cells or tissues, cells at different stages of differentiation, or tumor cells can be compared with their normal counterparts. The samples that are added to the microarray are usually not mRNA; reverse transcription is carried out on a matrix of total (total) mRNA, and the resulting cDNA is then labeled with a fluorescent material (fluorochrome). Fluorochromes of different colors are used to label cDNA from various sources.

On fig. Figure 5.15 shows how microarrays are used to compare gene expression in a population of tumor lymphoid cells and normal lymphocytes. Red fluorochrome was used as a label for experimental cDNAs from tumor cells, and green for cDNAs prepared from control normal analogs. Labeled cDNAs were applied to the chip and left to hybridize base pairs with the corresponding fragments. Both control and experimental cDNA were added to the microarray, so they competed for binding on the surface of the microarray.

Rice. 5.15. Microarray Study Comparing Tumor and Normal Lymphocyte mRNA Samples

The material that did not form hybrids was washed away, leaving fluorescent patches where the match occurred. At the end of hybridization, the microarray was scanned with a laser to detect red, green, or yellow spots. The highest levels of each type of cDNA reflected its color: red - cDNA of experimental tumor cells; green - control cDNA; yellow - the same levels of DNA in both samples. To interpret the results, the fluorescent scanner determined the exact fluorescence level of each spot on the glass.

The resulting data was then analyzed by a computer program that compared the fluorescence information with a genetic database to determine which genes were overexpressed or underexpressed in the tested samples. Characterization of the distribution and amount of DNA binding to a microarray has the potential to be useful in the field of immunology. In particular, for the clinical diagnosis of lymphoid tumors, the development of drugs (for example, testing immunosuppressive drugs under development for their effect on the expression of cytokine genes) and the discovery of new genes.

conclusions

1. In the interaction of an antibody and an antigen, covalent bonds are not used; weak forces such as electrostatic, hydrophobic and van der Waals forces are involved. Therefore, for sufficient interaction, the binding site of the antibody and the antigen must strictly match each other spatially, like a key with a lock.

2. Only a reaction between a polyvalent antigen and at least a divalent antibody can lead to an interaction expressed by cross-linking of antigen molecules by antibodies. These reactions are not possible with the participation of haptens or monovalent Fab fragments.

3. Interaction between soluble antibody and insoluble particulate antigen leads to agglutination. The degree of agglutination depends on the ratio of interacting antibodies and antigen. With a high concentration of antibodies, agglutination may not develop. This phenomenon is called prozone. The term "titre" means the highest dilution of serum at which agglutination still occurs, after which it does not begin at a higher dilution.

4. The precipitation reaction occurs by mixing in the correct ratio of soluble polyvalent antigen and (at least) divalent antibodies. It can take place in an aqueous medium or gel.

5. Gel reactions between soluble antigens and antibodies can be used to qualitatively and quantitatively analyze antibodies or antigens. Examples of such reactions are gel diffusion, radial diffusion, and immunoelectrophoresis.

6. Radioimmunoassay is a highly sensitive test for the quantitative determination of antigens or antibodies. It uses radioactively labeled antigens or antibodies, and the basis of the method is the competitive binding of unlabeled and labeled antigens. It is necessary to separate the antigen bound to the antibodies from the unbound labeled antigen. Typically separation is achieved using precipitation with anti-immunoglobulins.

7. Solid phase immunoassay is a technique that relies on the ability of many proteins to attach to plastic to form a monomolecular layer. The antigen is applied to the wells of the tablet, antibodies are added, then the wells are washed and the presence and amount of bound antibodies are measured, for which antiimmunoglobulins with a radioactive or enzyme label are used.

8. Enzyme immunosorbent assay is a type of solid phase immunoassay in which enzymes are attached to anti-immunoglobulins. The amount is determined by colorimetric evaluation after the addition of a substrate that changes color under the action of the enzyme.

9. Immunofluorescence is a method in which an antigen is detected using immunoglobulins labeled with fluorescein. With direct immunofluorescence, antibodies to the desired antigen carry a fluorescent label. With indirect immunofluorescence, antigen-specific antibodies are not labeled, they are determined after the addition of fluorescently labeled anti-immunoglobulins. Flow-through fluorescent cell sorters are instruments that can be used to enumerate and sort fluorescently labeled cells.

10. Assays used to evaluate lymphocyte function typically measure cell proliferative response or effector functions. For example, it is possible to examine the functional state of B cells by measuring their ability to proliferate and produce antibodies in response to B cell mitogens such as LPS or the pokeweed mitogen. T cells are usually examined for their ability to enhance the functions of other cells (in the case of CD4+ cells) or for their ability to destroy targets having specific antigens (in the case of CD8+ cells). In addition, T cells can be examined by measuring their ability to proliferate or produce certain cytokines in response to T cell mitogens such as PHA and Con A.

11. Monoclonal antibodies are highly specific reagents consisting of a homogeneous population of antibodies that are identical in specificity to a particular epitope.

R. Koiko, D. Sunshine, E. Benjamini

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disease immune infectious serological

1. T - lymphopoiesis, structure of antigen-recognizing receptors of T - lymphocytes, effector reactions of T - cells

Lymphopoiesis begins when pluripotent progenitors of T-blood cells pass from the bone marrow into the thymus cortex. Next, T-lymphocytes differentiate - they acquire specific markers of T-suppressors and T-helpers and migrate through the thymus medulla to secondary lymphoid organs (lymph nodes, spleen). Also, a small population of T-lymphocytes enters the bloodstream, bypassing the medulla. In the structures of the thymus, differentiation of T-lymphocytes occurs.

T-cell elements are a key link in the development of the body's immunological response. Mature T-lymphocytes are divided into a number of subclasses. They can "help" (helpers) or "suppress" (suppressors) the development of an immune response, including the formation of antibodies by B-lymphocytes. T-lymphocytes also perform effector functions, for example, the production of soluble substances that trigger a variety of inflammatory reactions, or the direct destruction of cells that carry antigens ("killer" function). In accordance with this, T-helpers, T-suppressors, T-killers, as well as T-cells involved in the delayed-type hypersensitivity reaction and related immunological phenomena are distinguished.

T-killers look for signs of viral infection and abnormalities (eg, malignant transformation) in other cells. When a T-killer precursor meets an antigenic complex (an antigen bound to a major histocompatibility complex (MHC) molecule on the surface of an infected cell, the prekiller undergoes multiple divisions. Daughter cells that carry receptors for this antigen become active killers and destroy cells infected with this virus. This makes it vulnerable to antibodies that bind viral particles.Antigen recognition by killer T-cells is specific.Specificity is due to T-cell receptors (TCRs).To fully activate the prekiller, it is not enough for the TCR to bind to the antigen complex.It is necessary to bind another molecule, the CD8 co-receptor. This protein is involved in antigen recognition by killer cells.Killer T-activation is most effective when TCR and CD8 bind to the same molecule.T-helper cells also have TCR and CD4 co-receptor, which together ensure the activation of T-helper cells. TCR and CD8 of killer cells bind to molecules class I histocompatibility class and peptides from proteins synthesized in the cell itself. TCR and CD4 helpers bind to class II histocompatibility proteins and antigenic peptides from proteins taken up by the cell. Helper T cells cooperate with B cells in an antibody response to antigens such as bacterial toxins. A toxic protein that enters the bloodstream is captured by a macrophage. B-lymphocytes also absorb toxin molecules bound to specific receptors such as antibodies on their surface. Inside macrophages and B-lymphocytes, the toxin is cleaved, and the resulting peptides are presented to the cell surface by histocompatibility class II proteins. T-lymphocytes begin to divide, forming active helpers, when TCR and CD4 bind to the same molecule of histocompatibility class II on the cell surface. Active helper T cells secrete interleukins that stimulate B lymphocytes to divide and secrete large amounts of antibodies. Free antibodies bind to the toxin and neutralize it.

Antigen-recognizing T-cell receptors - TCR (from the English - T cell receptor, TCR) consist of chains belonging to the immunoglobulin superfamily. The antigen-recognizing site of the TCR protruding above the cell surface is a heterodimer, i.e. it consists of two different polypeptide chains. Two types of T-cell antigen-recognizing receptors are known: bvTCR and gdTCR. These variants differ in the composition of the polypeptide chains of the antigen-recognizing site. Each T-lymphocyte expresses only 1 variant of the receptor. bvT-lymphocytes were discovered earlier and studied in more detail than gdT-cells.

The structure of the antigen-recognizing receptor of T-lymphocytes is best described using the example of bvTCR. The transmembranely located TCR complex consists of 8 polypeptide chains (a heterodimer of β- and β-chains of the TCR itself, two auxiliary chains g, and one heterodimer of the e/d- and e/r-chains of the CD3 molecule) (Fig. 1).

Rice. 1. Schematic of the T-cell receptor and related molecules

1) Transmembrane chains b and c TCR are 2 polypeptide chains of approximately the same size. Each of these chains contains 2 glycosylated domains in the extracellular part of the receptor, a hydrophobic transmembrane part, and a short (of 5-12 amino acid residues) cytoplasmic region. The extracellular parts of both chains are connected by a single disulfide bond.

2) The outer extracellular (distal) domains of both chains have a variable amino acid composition. They are homologous to the V region of immunoglobulin molecules and constitute the V region of the TCR.

3) The C-regions of the TCR are the proximal domains of both chains homologous to the constant regions of immunoglobulins.

4) A short cytoplasmic region ensures the conduction of a signal into the cell. For this, 6 additional polypeptide chains serve: d, d, 2e and 2g.

5) Chains r, e, e form heterodimers rhe and de between themselves. Together they form the CD3 complex. This complex is necessary for the expression of β- and β-chains, their stabilization, and signal transmission into the cell.

6) g-Chains are interconnected by a disulfide bridge. Most of these chains are located in the cytoplasm. These circuits conduct the signal inside the cell.

7) ITAM sequences. The cytoplasmic regions of the polypeptide chains d, e, f, and g contain 10 ITAM sequences that interact with Fyn, the cytosolic tyrosine kinase, whose activation initiates the onset of biochemical reactions for signal transduction.

Theoretically, each TCR is able to bind about 10 5 different antigens, not necessarily related in structure (cross-reacting), but not homologous in structure. However, in reality, TCR polyspecificity is limited to recognition of only a few structurally similar antigenic peptides.

2. Diseases of immune complexes, classification, features of the immune response

Immune complex disease (type III hypersensitivity) results from the deposition of soluble antigen-antibody complexes in tissues. Which leads to inflammation.

Damage in this type of allergic reaction is caused by antigen-AT immune complexes. In the body, reactions constantly occur with the formation of the AG-AT complex. These reactions are an expression of the protective function of the immune system and are not accompanied by damage. But under certain conditions, the AG-AT complex can cause damage and the development of the disease. Immune complexes are formed when there is an excess of antigen and antibodies. The concept that immune complexes (ICs) may play a role in pathology was proposed as early as 1905 by Pirke and Schick. Since then, a group of diseases in the development of which CI plays the main role has become known as immune complex diseases.

Immune complex diseases can be:

* systemic - which are caused by circulating antibodies (for example, serum sickness);

* local - as a result of the formation of immune complexes at the site of penetration of antibodies (for example, the Arthus phenomenon).

There may also be delayed allergic reactions involving Ig G class antibodies, which are also fixed on mast cells with the participation of the C3 complement component. They are also a manifestation of type 3 hypersensitivity reactions.

The conditions for the development of the immunocomplex mechanism of immunopathology are:

* the presence of a long-term (chronic) infectious process, involving the constant flow of antigens into the blood;

* the predominance of antibody reactions, i.e. the advantage of type 2 T-helpers, which control the development of the humoral immune response;

* relative insufficiency of the factors of destruction and elimination of the CEC from the bloodstream, namely, the complement system and the phagocytic reaction of neutrophils and macrophages;

* properties of the CEC. Pathogenic properties of the CEC are determined by the combination of their physicochemical properties, which include size, concentration, composition, solubility, and ability to fix complement. The molecular weight of the CEC determines their size, which is the most important indicator of pathogenicity. Also, the molecular weight determines the rate of CEC elimination from the body: large CECs are quickly eliminated and are relatively low pathogenic; small CECs are poorly eliminated, can be deposited subendothelially, are not able to activate the complement system; Medium-sized CECs are highly complement-binding and are the most pathogenic.

Immune complexes in the 3rd type of allergic reactions are deposited on the vascular wall or on the basement membranes. This deposition of immune complexes causes immune complex inflammation. Its essence is reduced to the activation of the classical pathway of the complement system with the formation of C3a-, C5a-complement components. They attract macrophages, neutrophils, mast cells to the site of the immune complex deposition, which determine tissue damage. In addition, intravascular deposits of immune complexes lead to platelet aggregation with the formation of microthrombi, which increase the accumulation of inflammatory mediators, resulting in the destruction of blood vessels and their replacement with connective tissue.

In the pathogenesis of immune complex reactions, the following stages are distinguished:

I. Immunological stage. In response to the appearance of an allergen or antigen, the synthesis of antibodies begins, mainly IgM and IgG classes. These antibodies are also called precipitating antibodies for their ability to form a precipitate when combined with the corresponding antigens. When AT is combined with AG, ICs are formed. They can be formed locally, in tissues or in the bloodstream, which is determined by the routes of entry or the place of formation of antigens (allergens). The pathogenic significance of CIs is determined by their functional properties and the localization of the reactions they cause.

II. pathochemical stage. Under the influence of IC and in the process of its removal, a number of mediators are formed, the main role of which is to provide conditions conducive to phagocytosis of the complex and its digestion. However, under unfavorable conditions, the formation of mediators can be excessive, and then they begin to have a damaging effect.

The main mediators are:

1. Complement, under conditions of activation of which various components and subcomponents have a cytotoxic effect. The leading role is played by the formation of C3, C4, C5, which enhance certain links of inflammation (C3v enhances the immune adhesion of IC to phagocytes, C3 and C4a play the role of anaphylatoxins).

2. Lysosomal enzymes, the release of which during phagocytosis enhances damage to basement membranes and connective tissue.

3. Kinins, in particular, bradykinin. With the damaging effect of IC, the Hageman factor is activated; as a result, bradykinin is formed from blood alpha globulins under the influence of kallikrein.

4. Histamine and serotonin play a large role in type III allergic reactions. Their source is mast cells, platelets and basophils. They are activated by the C3a and C5a complement components.

5. Superoxide anion-radical is also involved in the development of type III allergic reactions.

All of these mediators enhance proteolysis.

III. pathophysiological stage. As a result of the action of mediators, inflammation develops with alteration, exudation and proliferation. Vasculitis develops, leading to the appearance, for example, of glomerulonephritis. Cytopenias, such as granulocytopenias, may occur. Due to the activation of the Hageman factor and / or platelets, intravascular coagulation may occur.

The third type of allergic reactions is leading in the development of serum sickness, some cases of drug and food allergies, in some cases autoimmune diseases, etc. With significant complement activation, systemic anaphylaxis develops in the form of shock.

3. Phagocytosis and determination of phagocytic activity

Phagocytosis is a process in which specially designed cells in the blood and tissues of the body (phagocytes) capture and digest solid particles. The discovery of phagocytosis belongs to I. I. Mechnikov. It is carried out by two types of cells: granular leukocytes (granulocytes) circulating in the blood and tissue macrophages. In animals, oocytes, placental cells, cells lining the body cavity, and retinal pigment epithelium can also phagocytize.

The mechanism of phagocytosis is of the same type and includes 8 successive phases: 1) chemotaxis (directed movement of the phagocyte towards the object);

2) adhesion (attachment to an object);

3) activation of the membrane (actin-myosin system of the phagocyte);

4) the beginning of phagocytosis itself, associated with the formation of pseudopodia around the absorbed particle;

5) the formation of a phagosome (the absorbed particle is enclosed in a vacuole due to the pushing of the plasma membrane of the phagocyte on it like a zipper);

6) fusion of phagosomes with lysosomes;

7) destruction and digestion;

8) release of degradation products from the cell.

Phagocytosis is often preceded by the process of opsonization (from the Greek opsoniazo - to supply food, nourish) of the object. The object is a cell that carries alien information. The initiator of this process is the formation of an antigen-antibody complex on the cell surface. Antibodies, localized on the surface of a foreign cell, stimulate the activation and attachment of proteins of the complement system to them. The resulting complex acts as an activator of the remaining stages of phagocytosis.

In more detail, the stages of phagocytosis are as follows:

1. Chemotaxis. Foreign cells (opsonized or non-opsonized) send chemotactic signals to the environment, in the direction of which the phagocyte begins to move. Earlier than other cells, neutrophils migrate to the focus of inflammation, later - macrophages.

2. Adhesion of phagocytes to the object. It is due to the presence on the surface of phagocytes of receptors for molecules presented on the surface of the object (own or associated with it). The act of adhesion includes two phases: foreign recognition (specific process) and attachment, or actual adhesion (non-specific process). If there is no preliminary specific recognition of foreign cells, the adhesion of the phagocytic cell to the object of phagocytosis is extremely slow.

3. Membrane activation. At this stage, the object is prepared for immersion. There is an activation of protein kinase C, the release of calcium ions from intracellular depots. Sol-gel transitions in the system of cellular colloids and actin-myosin rearrangements are of great importance.

4. Dive. The object is wrapped. In the process of phagocytosis, the plasma membrane of the macrophage, with the help of the protruding folds formed by it, captures the object of phagocytosis and envelops it.

5. Formation of a phagosome. The membrane is closed, the object is immersed with a part of the phagocyte membrane inside the cell. The resulting small vacuole is called a phagosome.

6. Formation of phagolysosome. The fusion of phagosome with lysosomes, resulting in the formation of optimal conditions for bacteriolysis and splitting of the dead cell.

7. Killing and splitting. In the phagosome, the captured foreign cell dies. To carry out killing, the macrophage produces and secretes reactive oxygen derivatives into the phagosome. The main substances involved in bacteriolysis: hydrogen peroxide, products of nitrogen metabolism, lysozyme, etc. The process of destruction of bacterial cells is completed due to the activity of proteases, nucleases, lipases and other enzymes.

Digestion of the captured and killed material is the final stage of phagocytosis. For this, lysosomes, which contain more than 25 different enzymes, including a large number of hydrolytic enzymes, are combined with the phagosome containing the object of phagocytosis. In the phagosome, all these enzymes are activated, the so-called metabolic explosion, as a result of which the phagocytosed object is digested.

8. Release of degradation products.

Phagocytosis can be:

* completed (killing and digestion were successful);

* incomplete (for a number of pathogens, phagocytosis is a necessary step in their life cycle, for example, in mycobacteria and gonococci).

The study of phagocytosis indicators is important in the complex analysis and diagnosis of immunodeficiency states: often recurrent purulent-inflammatory processes, long-term non-healing wounds, and a tendency to postoperative complications.

For the study of phagocytic function, use:

* calculation of the absolute number of phagocytes (neutrophils and monocytes);

* assessment of the intensity of absorption of microbes by phagocytes;

* determination of the ability of phagocytic cells to digest captured microbes.

The most informative for assessing the activity of phagocytosis is the phagocytic number, the number of active phagocytes and the index of completeness of phagocytosis.

The most common method for quantifying and characterizing morphological defects in neutrophils is a leukogram and cytological studies using light and electron microscopy.

To determine the chemotactic activity of neutrophils, the method of studying the migration of leukocytes using a Boyden camera is used. The method is based on the separation by a microporous filter in a solution of two reacting components: neutrophils and chemotactic agents (for example, C5a), which are placed in the lower chamber and create a concentration gradient. Neutrophils placed in the upper chamber migrate along the gradient and collect on the lower surface of the filter. After the standard incubation, the filters are removed, stained and the cells counted. The method is quite simple and has a very high reproducibility. The same principle underlies the cell migration method under agarose gel, which is used to determine the chemotactic index.

For the phagocytic number, the norm is 5-10 microbial particles. This is the average number of microbes absorbed by one blood neutrophil. Characterizes the absorption capacity of neutrophils. Determined by counting the number of absorbed bacteria per cell after incubation of the patient's cells with standard preparations of St.aureus or E.coli and staining of the resulting smears. A modification of this test is a method for determining bactericidal activity, in which the washed cell suspension is incubated with a bacterial suspension, then the mixture is applied to the surface of blood agar, and after a certain time the number of grown bacterial colonies is counted. Both methods require standardization for use in each specific laboratory and information about antibiotic therapy, which may cause unreliable results or errors in their interpretation.

The phagocytic capacity of blood is normal - 12.5-25x10 9 per 1 liter of blood. This is the number of microbes that neutrophils can absorb in 1 liter of blood.

The phagocytic index is normal 65-95%. This is the relative number of neutrophils (expressed as a percentage) involved in phagocytosis.

The number of active phagocytes in the norm is 1.6-5.0x10 9 in 1 liter of blood. This is the absolute number of phagocytic neutrophils in 1 liter of blood.

The index of completeness of phagocytosis is normally more than 1. It reflects the digestive capacity of phagocytes.

The phagocytic activity of neutrophils usually increases at the beginning of the development of the inflammatory process. Its decrease leads to the chronicity of the inflammatory process and the maintenance of the autoimmune process, since this disrupts the function of destruction and removal of immune complexes from the body.

Spontaneous test with NBT (nitrosine tetrazolium) - normally in adults, the number of NBT-positive neutrophils is up to 10%. This test allows you to assess the state of the oxygen-dependent mechanism of bactericidal activity of phagocytes (granulocytes) of blood in vitro. It characterizes the state and degree of activation of the intracellular NADP-N-oxidase antibacterial system. The phenomenon of a respiratory (or metabolic) explosion is associated with a significant increase in oxygen absorbed by leukocytes during phagocytosis, resulting in the formation of superoxide radical (O 3 -) and hydrogen peroxide. All these compounds have microbicidal properties, and their identification is an important step in assessing the functional activity of phagocytic cells.

Indicators of the NBT-test increase in the initial period of acute bacterial infections, while they decrease in the subacute and chronic course of the infectious process.

A decrease in the spontaneous test with NST is characteristic of chronic inflammation, congenital defects of the phagocytic system, immunodeficiencies, malignant neoplasms, severe burns, injuries, malnutrition, treatment with certain drugs, exposure to ionizing radiation.

An increase in the spontaneous test with NBT is noted with antigenic irritation due to acute bacterial inflammation, leukocytosis, increased antibody-dependent cytotoxicity of phagocytes, autoallergic diseases, and allergies.

The activated test with NBT is used to determine the phagocytic metabolic (oxygen-dependent) activity of neutrophils. The test includes the incubation of neutrophils with NBT in vitro, and the formation of insoluble colored formazan granules can be judged on the reduction of NBT by the superoxide radical formed during the activation of phagocytes. The absence of sediment indicates the inability of the cell population of phagocytes to metabolism.

Normally, in an adult, the number of NBT-positive neutrophils is 40-80%. A decrease in the activated NBT test of neutrophils below 40% and monocytes below 87% indicates a lack of phagocytosis.

4. Analyze the results of serological methods for diagnosing infectious animal diseases using the example of the work of a veterinary laboratory (district, regional, interdistrict)

Regional veterinary laboratory in the federal state institution "Egorievsk regional veterinary laboratory" in the Moscow region.

Head of the veterinary laboratory Novikov O.P., veterinarian of the serological department Ivanova T.N.

The activities of the laboratory are aimed at ensuring the prevention and elimination of animal diseases, at protecting the population from diseases common to humans and animals, as well as the production of high-quality products and raw materials of animal origin.

The laboratory carries out bacteriological, biochemical, serological, pathoanatomical, toxicological, caproscopic and other laboratory methods for the study of relevant materials coming from veterinary institutions of the region or directly from farms.

Table 1 - Veterinary laboratory report (December 2012 to November 2013) on testing for viral diseases

Name of the disease, animal species, test material indicator

Material quantity

Research done

Received positive results

pathological

microscopic

Virological

biological

serological

Histological

hematological

Light

Luminescent

adenovirus infection

Rabies Commercial and wild animals, pathological material

Dogs, patmaterial

Cats, patmaterial

Other types of pat material

bovine viral diarrhea

Equine infectious anemia

Infectious rhinotracheitis

Bovine leukemia WBC count

Derived leukoformula

Dog serum

swine pox

brucellosis swine

A serological test is a blood serum test that allows you to identify infected animals. As can be seen from Table 1, the following serological methods are most widely used in this laboratory: agglutination test (RA) and complement fixation test (CFR) in the diagnosis of precellosis; diffuse precipitation test (RDP) in the diagnosis of equine infectious anemia.

In order to evenly load the laboratories, mass serological, caproscopic, allergic tests are carried out by the laboratory according to the appropriate calendar plan agreed with the chief veterinarian of the district.

The laboratory studies the epizootic and veterinary and sanitary conditions of farms in the assigned zone, and tests new diagnostic preparations.

The laboratory advises veterinary institutions, veterinary specialists and farm workers on the prevention and eradication of animal diseases.

When particularly dangerous diseases are detected, the laboratory determines the nature, scope and procedure of diagnostic studies, conducts their detection in a short time, and, if necessary, sends its specialists to clarify the diagnosis on the spot and determine the extent of the spread of the infection.

List of sources used

1. Ado, A.D. About some properties and interaction of receptors of membranes of lymphocytes/A. D. Ado. // Immunology. - 1993. - No. 6. - 12-17 p.

2. Belousova, R.V. Veterinary virology: a textbook for universities on special. "Veterinary" / R.V. Belousova, E.A. Preobrazhenskaya, I.V. Tretyakova; ed. R.V. Belousova; int. assoc. "Agriculture". - M. : KolosS, 2007. - 422 p.

3. Voronin, G.S. Immunology / G.S. Voronin, A.M. Petrov, M.M. Serykh, D.A. Dervishov. - M.: Kolos-Press, 2002. - 408 p.

4. Zykin, L.F. Clinical microbiology for veterinarians: a textbook for universities on special. "Veterinary" / L.F. Zykin, Z.Yu. Khaptsev. - M.: KolosS, 2006. - 95s.

5. Kislenko, V.N. Veterinary microbiology and immunology: a textbook for universities on special. "Veterinary" Part 3: Private microbiology / V.N. Kislenko, N.M. Kolychev, O.S. Suvorina; int. association "Agriculture". - M.: KolosS, 2007. - 214 p.

6. Kislenko, V.N., Kolychev, N.M., Gosmanov, R.G. Veterinary microbiology and immunology / V.N. Kislenko, N.M. Kolychev, R.G. Gosmanov. - GEOTAR-Media, 2012.- 784 p.

7. Kolyakov, Ya.E. Veterinary immunology / Ya.E. Kolyakov. - M.: Agropromizdat, 1987.-340 p.

8. Kondrakhin, I.P. and others. Clinical laboratory diagnostics in veterinary medicine: a Handbook / I.P. Kondrakhin, N.V. Kurilov, A.A. Malakhov, etc. - M .: Agropromizdat, 1985 - 150 p.

9. Skorodumov, D.I. Microbiological diagnosis of bacterial animal diseases: a reference book / D.I. Skorodumov [and others]. - M. : Izograph, 2005. - 652 p.

10. Terekhov, O.P. Immune system - endogenous nutrition system of multicellular organisms / O.P. Terekhov. //Immunology. - 2005. - No. 1. -59-62 p.

11. http://www.booksmed.com/allergologiya-immunologiya/2171-immunologiya-yarilin-a.a.-uchebnik.html

12.http://www.medn.ru/statyi/fagocitoz.html

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