What does hypersensitivity mean? Hypersensitivity to drugs: causes, symptoms, diagnosis, treatment

Allergy (from Greek allos - different, ergon - I act) - this is a state hypersensitivity(sensitization) to substances with antigenic properties or even without them. Currently 30 - 40% of the population developed countries susceptible to allergies.

The term “allergy” was introduced in 1905 by K. von Pirke to designate a special excessive reaction of the body to contact with an antigen. In 1902, Richet and Portier (Pasteur Institute) discovered the phenomenon in an experiment on dogs anaphylactic shock. This was the beginning of allergology.

Antigens that cause an allergic reaction are called allergens . Types of allergens:

  • household (household book dust is a waste product of house mites);
  • epiallergens (hair, wool, skin, scales);
  • simple chemical substances;
  • hay fever (plant pollen);
  • medicinal substances (antibiotics, sulfonamide drugs);
  • food allergens;
  • infectious allergens (antigens of microorganisms);
  • autoallergens (primary - antigens of cells of those organs to which innate immunological tolerance has not been formed (brain, thyroid and gonads, eye tissues; secondary - macromolecules of cells with an altered structure as a result of a burn, radiation sickness, frostbite, etc.)).
95% of people are allergic to one allergen, that is, they are monoallergenic. Children, as a rule, are polyallergenic.

Types of hypersensitivity. Hypersensitivity reactions are classified into hypersensitivity immediate type(HNT) and delayed type (HRT) depending on the time of appearance of symptoms after the re-encounter of the sensitized organism with the allergen (Table 1).

Table 1

Characteristics of hypersensitivity reactions


Sign GNT,

B-type reactions

 HRT,

T-type reactions
Time after reintroduction of allergen A couple of minutes 5 - 7h, maximum 12 - 24h
Allergens Proteins, polysaccharides Transplanted tissues, chemicals, tuberculin, autoallergens
Antibodies in the blood Present None
Transfer to another

To the body

 Serum and lymphocytes Only lymphocytes
Desensitization Effective Ineffective
Clinical

Manifestations

 Anaphylactic shock, atopies (uncommon): migraine, hay fever, urticaria, bronchial asthma tuberculin type reactions, autoimmune reactions, transplant rejection

HNT, like HRT, occurs in 3 stages:
  1. immunological,
  2. pathochemical,
  3. pathophysiological.
The essence of the immunological stage is the production of antibodies and sensitized lymphocytes. During the immunological stage, an accumulation of allergen occurs, which is fixed on the surface of mast cells connective tissue(mediator containers). Antibodies or sensitized lymphocytes accumulate on the 12th - 14th day.

The pathochemical stage is characterized by the release of substances - mediators - into the blood allergic reactions. At reintroduction allergen, it combines with antibodies on the surface of mast cells, which thereby become irritated, excited and release mediators into the blood. Characteristics of the main mediators of allergic reactions are given in Table. 2.

table 2

Main mediators of allergic reactions


Mediator Chemical nature Biological effect
Histamine Amine derivative

Histidine

 Narrowing coronary arteries and bronchi, increasing capillary permeability, suppressing the activity of T-lymphocytes, limiting further activation of mast cells
Serotonin Amine, tryptophan derivative Activation of blood clotting processes, constriction of cerebral vessels
Heparin Heteropolysaccharide Decreased blood clotting
Slow reacting substance of anaphylaxis (MRSA) Complex of leukotrienes - derivatives of arachidonic acid Thrombosis, vasodilation, stimulation of histamine and bradykinin formation
Bradykinin Peptide Dilatation of arteries, reduction blood pressure, stimulation of histamine release

Rice. 16. Development of an allergic reaction

The content of the pathophysiological stage of allergy consists of changes in activity various organs under the influence of allergy mediators. The mediator dilates small vessels, increases their permeability, causing spasm smooth muscle, increases the secretion of mucous glands respiratory system, digestive tract. There is spasm of the bronchi and intestines, a drop in blood pressure, and a rash of red spots on the skin. The location of the process determines the symptoms. If it's subcutaneous fatty tissue, then itching is not observed, if the superficial layers of the skin (urticaria), then itching appears, since there are pain receptors in the skin.

A more complex classification of allergic reactions was proposed by Coombs and Gell. They identified four types of hypersensitivity (types I, II, III and IV). This classification takes into account three criteria: location of the allergen, location of the antibody, participation in the complement reaction. Reactions of the first three types are mediated by antibodies, reactions of the fourth - mainly by T cells and macrophages.

Type I reactions (reagin) . Upon contact with normally harmless antigens (allergens) environment, for example with pollen, animal dander and house dust mites, IgE is produced, called reagins . IgE binds to specific receptors on mast cells in connective tissue. When an allergen interacts with IgE associated with mast cells, the latter release mediators that cause clinical symptoms allergies. Typical examples of allergic reactions are hay fever, asthma, atopic eczema, drug allergy and anaphylaxis. They are used for their treatment antihistamines, bronchodilators, adrenaline, corticosteroids and specific immunotherapies.

Pollutants external environment increase the level of antigen-specific IgE. Environmental pollutants such as sulfur dioxide (sulfur dioxide), nitrogen oxides, airborne diesel exhaust particles (DEP) and ash can increase the permeability of mucous membranes, facilitating the penetration of allergens into the body and the occurrence of IgE reactions. PDV can play the role of a powerful adjuvant that enhances IgE production. The diameter of these particles is less than 1 micron; they persist for a long time in the atmosphere of polluted cities and affect Airways. The BPV concentration in city air averages approximately 1 μg/m 3 , and on main highways it can reach 30 μg/m 3 , increasing to 500 μg/m 3 during periods of particularly heavy traffic. When PDV is inhaled along with an antigen, the content of antigen-specific IgE increases sharply. This adjuvant effect also occurs at low concentrations of the antigen, comparable to those present in the environment.

The incidence of allergic rhinitis and asthma has been increasing over the past 30 years in parallel with the increase in air pollution. Thus, environmental pollutants that promote the IgE response may contribute to the increasing prevalence of allergic diseases.

If so many are associated with IgE negative effects, the question arises: why did antibodies of this class appear in evolution at all? In the process of evolution, antibodies of the IgE class appeared, possibly to protect the body from helminths (since approximately a third of the entire population globe infected with helminths). The production of IgE in response to allergens with the subsequent development of an allergic reaction can be considered an undesirable side effect.

Type II reactions (antibody-dependent cytotoxic) occur when antibodies, usually of the IgG class, bind on the surface of cells to self or foreign antigen, resulting in phagocytosis, killer cell activation, or complement-mediated lysis. A classic example of these reactions is autoimmune hemolytic anemia, as well as hemolysis during transfusion incompatible blood.

Type III reactions (immunocomplex) develop during education large quantity immune complexes or if their elimination by the reticuloendothelial system is impaired. In this case, complement activation occurs, and polymorphonuclear cells accumulate at the site of complex deposition, causing local tissue damage and inflammation.

Type IV reactions (delayed hypersensitivity or DTH) It is most pronounced in cases where macrophages absorb foreign material (for example, tuberculosis pathogens), but are not able to eliminate it. In this case, the synthesis of cytokines by T cells is stimulated, causing various inflammatory reactions. Other manifestations of HRT reactions include graft rejection and allergic contact dermatitis.

The reaction of the immune system to the effects of various components of origin that enter the body with air, food, during contact with the skin, or as a result drug treatment called hypersensitivity.

The causes of hypersensitivity are disorders immune functions body. Hypersensitivity reactions are triggered by many antigens and the causes vary from person to person.

Classify hypersensitivity reactions using immunological mechanisms that cause them.

There are two forms of hypersensitivity reaction:

  • immediate type hypersensitivity, which includes 3 types of hypersensitivity (I, II, III);
  • delayed type hypersensitivity - type IV.

Diagnosis of immediate types of reactions

  1. Allergological history. It is necessary to collect the information needed to carry out diagnosis and treatment.
  2. Comprehensive physical examination. The respiratory organs, skin, eyes, and chest are subject to careful examination.
  3. Laboratory research, thanks to which it is possible to refute or confirm the diagnosis that was made based on the results of the anamnesis, as well as taking into account physical examinations. Laboratory tests also help in assessing the effectiveness of treatment and help monitor the patient’s condition.
  4. General analysis blood.
  5. Sputum smears.
  6. Skin tests.
  7. General level immunoglobulins IgE in serum.
  8. Provocative tests. This method is based on the introduction of allergens into the target organ, it allows you to identify sensitization.
  9. Conducting respiratory function studies. This method is used to carry out a differential diagnosis of non-allergic and allergic lung diseases in order to assess the reactivity of the bronchi and the severity of these diseases, as well as the effectiveness of their treatment.
  10. X-ray examination.

Diagnosis of delayed types of reactions

The following methods are used to diagnose these types of hypersensitivity reactions:

  • determination of the level of serum immunoglobulins IgE;
  • conducting skin and provocative tests using suspected allergens,
  • determination of sensitized cells using tests, carrying out the blast transformation reaction of lymphocytes,
  • carrying out a migration inhibition reaction in leukocytes;
  • carrying out cytotoxic tests.

Anaphylactic reactions - type 1 reactions

This reaction is based on the mechanism of tissue damage, which usually occurs with the participation of immunoglobulins E and G. B in this case biologically penetrate into the blood active substances(serotonin, histamine, heparin, bradykinins and others). In this case, there is an increase in secretion, a violation of membrane permeability, muscle spasm, and interstitial edema.

Hypersensitivity reactions of this type are divided into local and systemic.

Local reactions completely depend on the site of entry of the antigen.

Symptoms of the disease:

  • anaphylactic shock;
  • conjunctivitis and nasal discharge;
  • swelling of the skin;
  • hay fever and bronchial asthma;
  • allergic gastroenteritis.

A systemic reaction usually develops in response to intravenous administration of an antigen to which the host is already sensitized. After a few minutes, a state of shock may develop. This condition can be fatal.

This type of hypersensitivity reaction goes through two phases in development. Symptoms of the first phase:

  • dilation of blood vessels, as well as increasing their permeability;
  • secretion of glands or spasm of smooth muscles.

These symptoms appear 5-30 minutes after administration of the antigen.

The second phase often begins to develop after 2-8 hours and can last several days.

Late phase symptoms:

  • intense infiltration of neutrophils, eosinophils, basophils and monocytes.
  • tissue destruction.

Cytotoxic reactions - reactions of the second type

Circulating antibodies react with components membranes of tissues and cells. This type of reaction occurs with the participation of immunoglobulins G, M, and also during activation of the complement system. As a result, it is damaged cell membrane. This type reactions appear with thrombocytopenia, hemolytic disease newborns with Rh conflict, allergies, hemolytic anemia.

During this type of hypersensitivity reaction, antibodies appear in the body directed against antigens that are located on the surface of cells or other tissue components.

There are two ways in which antibodies can cause a type 2 hypersensitivity reaction: opsonization and direct lysis.

Clinical hypersensitivity reactions of type II occur in the following cases:

  • during transfusion of incompatible blood, in which the donor’s cells react with the host’s antibodies;
  • during erythroblastosis of the fetus, there is an antigenic difference between the fetus and the mother, and maternal antibodies, penetrating the placenta, can cause the destruction of red blood cells in the fetus;
  • during thrombocytopenia, anemia and agranulocytosis, in which antibodies are formed against one’s own blood cells, which are then destroyed;
  • During some reactions to drugs, antibodies form when reacting with the drugs.

Immune complex reactions - hypersensitivity reactions of the third type

The third type of hypersensitivity reaction is caused by the formation of precipitating antibody-antigen complexes in a small excess of antigens. The complexes, deposited on the walls of blood vessels, activating the complement system, thereby causing inflammatory processes, such as serum sickness, immune complex nephritis. The reaction mechanism is closely related to tissue damage by immune complexes and involves immunoglobulins G and M. This type of reaction is characteristic of allergic dermatitis, exogenous allergic conjunctivitis, systemic lupus erythematosus, immune complex glomerulonephritis, rheumatoid arthritis, serum sickness.

There are 2 types of immune complex lesions:

  1. when exogenous antigens, such as proteins, bacteria, viruses, enter the human body;
  2. during the formation of antibodies against self-antigens

Immune cell reactions - reactions of the fourth type

This type of reaction is caused by contact of a specific antigen with T lymphocytes. After repeated contact with the antigen, T-cell-dependent delayed inflammatory reactions begin to develop, which can be local or generalized. This, for example, could be allergic contact dermatitis. Any organs and tissues can be involved in the process. This type of reaction is characteristic of diseases such as brucellosis and tuberculosis.

Treatment of hypersensitivity reactions

Treatment consists of a number of activities. The most important thing is to stop exposure to the allergen. To do this, it is necessary to isolate the patient from animals, install air conditioners with filters, and give up many medications and foods. If it is impossible to completely eliminate the allergen, then you need to reduce its intensity of exposure.

Antihistamines are also used for treatment.

Substances and products that seem familiar at first glance can cause a violent and sometimes unpredictable reaction in the body. Hypersensitivity is the reaction of the immune system to the effects of components of various origins that enter the body with food, air, contact with the skin or as a result of drug treatment. Reason of this disease Various disorders of the body's immune functions are considered. The immune system reacts to the penetration of foreign substances by releasing antibodies aimed at neutralizing and destroying allergens. This process is accompanied by the release of histamine with the formation of swelling, inflammation and itching. skin. The severity of the reaction may be moderate or dangerous character in the form of shock (anaphylaxis).
Allergens such as pollen can cause hypersensitivity reactions various plants, animal fur, household dust, waste products of fleas, dust mites. Manifestations of a reaction to such irritants may include asthmatic attacks and shortness of breath. The foods that most often cause allergic reactions are milk, eggs, fruits, nuts and chitinous shellfish (crayfish, crabs, lobsters). A food allergic reaction, as a rule, is manifested by a disorder of the skin (peeling, dryness, redness, contact dermatitis, atopic eczema), but digestive disorders also occur. Contact dermatitis is a consequence of skin hypersensitivity to various stimuli(metals, cosmetical tools, washing powders, rubber, cement mortars). Sensitivity to insect stings (wasps, bees, etc.) and medicines(sulfonamides, aspirin) may cause severe reaction body, manifested by the onset of anaphylactic shock and damage to cells of the brain, liver, and kidneys. The onset of this condition requires emergency medical intervention.
Diagnosis of predisposition to hypersensitivity and identification of allergens that provoke this condition are carried out using a skin prick test. The suspected irritant is applied to a previously damaged area of ​​skin and the reaction determines whether the substance is an allergen or not. If an allergen is identified, contact with this substance must be avoided in every possible way. Some types of hypersensitivity can be treated by taking medications that suppress (reduce) immune reaction through regular administration of minimal doses of the allergen. Heavy states of shock(swelling, breathing spasms) are eliminated by injections of hormonal and antihistamines.
Basically, the tendency to a certain hypersensitivity is genetic and is inherited. The state of the environment, social situation and lifestyle can be considered factors influencing the appearance and development of this disease.

Updated: 2019-07-09 23:52:34

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Lecture 17

REACTIONSHYPERSENSITIVITY

Hypersensitivity reactions can be classified based on the immunological mechanisms that cause them.

In type I hypersensitivity reactions, the immune response is accompanied by the release of vasoactive and spasmogenic substances that act on blood vessels and smooth muscles, thus disrupting their functions.

In type II hypersensitivity reactions, humoral antibodies are directly involved in cell damage, making them susceptible to phagocytosis or lysis.

In type III hypersensitivity reactions (immune complex diseases), humoral antibodies bind antigens and activate complement. Complement fractions then attract neutrophils, which cause tissue damage.

In type IV hypersensitivity reactions, tissue damage occurs, which is caused by the pathogenic effect of sensitized lymphocytes.

Type I hypersensitivity reactions - anaphylactic reactions

Type I hypersensitivity reactions can be systemic or local. A systemic reaction usually develops in response to intravenous administration an antigen to which the host is already sensitized. In this case, a state of shock often develops after a few minutes, which can cause death. Local reactions depend on the place where the antigen enters and are in the nature of localized swelling of the skin ( skin allergy, urticaria), discharge from the nose and conjunctiva (allergic rhinitis and conjunctivitis), hay fever, bronchial asthma or allergic gastroenteritis (food allergy).

Scheme25. ReactionshypersensitivityItype- anaphylacticreactions

It is known that type I hypersensitivity reactions undergo two phases in development (Scheme 25). The first phase of the initial response is characterized by vasodilation and an increase in their permeability, as well as, depending on the location, spasm of smooth muscles or glandular secretion. These signs appear 5-30 minutes after exposure to the allergen. In many cases, the second (late) phase develops after 2-8 hours, without further

additional antigen exposure and lasts several days.

Mast cells and basophils play a major role in the development of type I hypersensitivity reactions; they are activated by cross-reacting high-affinity IgE receptors. In addition, mast cells are activated by complement components C5a and C3 (anaphylatoxins), as well as macrophage cytokines (interleukin-8), some medicinal substances

(codeine and morphine) and physical influences (heat, cold, sunlight).

In humans, type I hypersensitivity reactions are caused by immunoglobulins of the IgE class. The allergen stimulates the production of IgE by B lymphocytes mainly in the mucous membranes at the site of antigen entry and in regional lymph nodes. IgE antibodies formed in response to an allergen attack mast cells and basophils, which have highly sensitive receptors for the Fc portion of IgE.

After mast cells and basophils, attacked by cytophilic IgE antibodies, re-encounter a specific antigen, a series of reactions develops, leading to the release of a number of strong mediators responsible for the clinical manifestations of type I hypersensitivity. First, the antigen (allergen) binds to IgE antibodies. In this case, multivalent antigens bind more than one IgE molecule and cause cross-linking of neighboring IgE antibodies.

- The binding of IgE molecules initiates the development of two independent processes: 1) degranulation of mast cells with the release of primary mediators; 2) de novo synthesis and release of secondary mediators, such as arachidonic acid metabolites. These mediators are directly responsible for

- Enzymes are contained in the granule matrix and include proteases (chymase, tryptase) and some acid hydrolases. Enzymes cause the formation of kinins and the activation of complement components (C3), affecting their precursors - Proteoglycan- heparin.

Secondary mediators include two classes of compounds; lipid mediators and cytokines. - Lipid mediators

are formed due to sequential reactions occurring in the membranes of mast cells and leading to the activation of phospholipase A2. It affects membrane phospholipids, causing the appearance of arachidonic acid. Arachidonic acid, in turn, produces leukotrienes and prostaglandins.

Leukotrienesplay an extremely important role in the pathogenesis of type I hypersensitivity reactions. Leukotrienes C4 and D4 are the most powerful vasoactive and spasmogenic agents known. 2 They are several thousand times more active than histamine in increasing vascular permeability and contracting bronchial smooth muscle. Leukotriene B4 has a strong chemotactic effect on neutrophils, eosinophils and monocytes. Prostaglandin D

is formed in mast cells and causes intense bronchospasm and increased secretion mucus. Platelet activating factor (FAT) is a secondary transmitter that causes platelet aggregation , histamine release, bronchospasm, increased vascular permeability and dilation blood vessels . In addition, it has a pronounced pro-inflammatory effect. PAF has a toxic effect on neutrophils and eosinophils.. TNF-α is considered a strong proinflammatory cytokine that can attract neutrophils and eosinophils, promoting their penetration through the walls of blood vessels and activating them in tissues. Finally, IL-4 is required for eosinophil recruitment. Inflammatory cells accumulating in places where a type I hypersensitivity reaction develops

pa, are additional source cytokines and gnetamine-releasing factors, which cause further degranulation of mast cells.

Thus, histamine and leukotrienes are rapidly released from sensitized mast cells and are responsible for the immediately developing reactions characterized by edema, mucus secretion, and smooth muscle spasm.

Many other mediators are represented by leukotrienes, PAF and TNF-a. are included in the late phase of the response, recruiting additional numbers of leukocytes - basophils, neutrophils and eosinophils.

Among the cells that appear in the late phase of the reaction, eosinophils are especially important. The set of mediators in them is as large as in mast cells. Thus, additionally recruited cells enhance and maintain the inflammatory response without additional antigen supply. Regulation of hypersensitivity reactions of type I by cytokines. Firstly, IgE secreted by B lymphocytes in the presence of IL-4 plays a special role in the development of type I hypersensitivity reactions. YYA-5

and IL-6, and IL-4 is absolutely necessary for the transformation of IgE-producing B cells. The propensity of some antigens to cause allergic reactions is due in part to their ability to activate T helper 2 (Th-2) cells. On the contrary, some cytokines. formed by T-helper-1 (Th-I), for example gamma interferon (INF-γ). reduce IgE synthesis. Secondly, a feature of type I sensitivity reactions is increased content Sensitization– is an immunologically mediated increase in the body’s sensitivity to antigens (allergens). There are two known forms of hypersensitivity reactions (increased reactivity ):immediate hypersensitivity(manifestation of humoral immunity ); delayed type hypersensitivity (manifestation of cellular immunity).

Immediate hypersensitivity is realized with the participation of antibodies acting on mast cells and basophils that produce inflammatory mediators.

Delayed-type hypersensitivity is carried out with the help of T cells, which ensure the accumulation of macrophages in the area of ​​inflammation. Depending on the immunological mechanisms underlying them, hypersensitivity reactions of types I, II, III and IV are distinguished. I, II and III types– immediate type hypersensitivity reactions, IV – delayed type.

TYPE I REACTIONS (ANAPHYLAXIA)

Anaphylaxis(from the Greek ana - again and phylaxis - defenselessness) - an acutely developing type of immunological reaction caused by the interaction of the allergen with IgE fixed on the membranes of mast cells and basophils. Type I hypersensitivity reactions include two stages - an initial response and a late response. The initial response phase develops 5-30 minutes after contact with the allergen and is accompanied by vasodilation, increased permeability, spasm of smooth muscles, and hypersecretion of glands. The late phase is observed after 2-8 hours without additional contact with the antigen, lasts several days and is characterized by intense tissue infiltration by eosinophils, neutrophils, basophils and monocytes, T-helpers, as well as damage to epithelial cells of the mucous membranes. The development of type I hypersensitivity is ensured by IgE antibodies formed in response to an allergen with the participation of T2 helper cells. Antibodies are adsorbed on mast cells and basophils. Upon repeated contact of mast cells and basophils sensitized by IgE antibodies with a specific antigen, an immediate release of mediators occurs, causing clinical manifestations. Type I hypersensitivity reactions can be systemic or local. A systemic reaction develops in response to intravenous administration of an antigen to which the host’s body is previously sensitized, and can be of the nature of anaphylactic shock. Systemic anaphylaxis occurs after the administration of heterologous proteins - antisera, hormones, enzymes, polysaccharides, and some drugs (penicillin). This is the most severe form of allergic reactions and is classified as an emergency. medical conditions. The severity of the condition depends on the level of preliminary sensitization. The shock dose of antigen can be very small. A few minutes after contact with the antigen, itching, urticaria and skin erythema appear, angioedema, then through a short time are developing respiratory disorders– shortness of breath, rhinorrhea, bronchospasm, vomiting, abdominal cramps, diarrhea and laryngeal edema. These symptoms may result in shock with vascular collapse, tachycardia, neuropsychiatric disorders and death of the patient. At autopsy, in some patients, swelling and hemorrhages are found in the lungs, in others - acute emphysema lungs with dilatation of the right ventricle of the heart. Local anaphylaxis occurs when it enters the body in the respiratory tract, gastrointestinal tract, on the skin of allergens - plant pollen, animal dander, house dust, etc. Local reactions depend on the site of penetration of the antigen and have the character of limited swelling of the skin (skin allergies, urticaria), discharge from the nose and conjunctiva ( allergic rhinitis, conjunctivitis), hay fever, bronchial asthma or allergic gastroenteritis (food allergy).

TYPE II REACTIONS (CYTOTOXIC REACTIONS)

Type II reactions develop when antibodies (IgM or IgG) interact with an antigen located on the surface of cells. This leads to damage to the cell or tissue. The antigen can be not only exogenous, but also its own, which is accompanied by damage to its cells. Cytotoxic reactions occur in several ways. Activation of complement, causing lysis of the cell membrane and its death. Phagocytosis – the antigen-bearing cell is engulfed by macrophages, which recognize antigen-antibody complexes on the cell. Cellular cytotoxicity - the antigen-antibody complex is recognized by killer cells (K cells), which destroy the cell. K cells include granulocytes, macrophages, platelets, NK cells (natural killer cells). Changing cell function - an antibody can react with cell surface molecules or receptors, affecting its function, but without causing its necrosis. In the clinic, type II reactions are observed during transfusion of incompatible blood, with hemolytic disease of the newborn, with reactions to drugs, myasthenia gravis, and Graves' disease.

TYPE III REACTIONS (IMMUNOCOMPLEX REACTIONS)

The damage in this type of hypersensitivity is caused by antigen-antibody complexes. Immune complexes can form at the site of antigen localization (immune complexes in situ). In this case, damage to one organ occurs, as for example in post-streptococcal glomerulonephritis. The formation of immune complexes in the circulatory system contributes to multiorgan pathology (systemic lupus erythematosus, polyarteritis nodosa). Immune complex diseases are also caused by drugs (penicillin, sulfonamides), food products(milk, egg whites), inhalation allergens (house dust, fungi), bacterial and viral antigens. The morphological picture of immune complex damage is dominated by acute necrotizing vasculitis, which leads to the development of local hemorrhages, but thrombosis is more often observed, contributing to the development of local ischemic damage.

TYPE IV REACTIONS (DELAYED TYPE HYPERSENSITIVITY – CELLULAR REACTIONS)

TRANSPLANT REJECTION

The graft rejection reaction is associated with the recognition by the host of the transplanted tissue as foreign. Responsible for such rejection HLA antigens. Transplant rejection – difficult process, during

of which both cellular immunity and circulating antibodies are important. Transplantation is the process of transferring cells, tissues, organs from one place to another. The immune system has very powerful mechanisms that counteract foreign agents, including foreign tissue. These mechanisms are involved in graft rejection reactions. Below are the main types of transplantation. Autotransplantation is a tissue transplantation within one organism (almost always successful). Syngeneic transplants are tissues that are genetically closely related to the donor (for example, obtained from identical twins or inbred animals). Allogeneic grafts are tissues transplanted from one individual to another genetically alien individual of the same species. Xenogeneic grafts are tissues transplanted from an individual of another species (usually subject to rejection). Types of transplant rejection: hyperacute (developing on the 1st day of transplantation); acute (developing during the first four weeks after transplantation); chronic (developing from a month to several years after transplantation). Transplant rejection occurs with the participation of killer T cells (CD8+) and helper T cells (CD4+). With the participation of T-helpers, specific T-killers and plasma cells are formed. Subsequently, there is an accumulation of effector cells coming from the lymphoid organs in the graft. The transplant is rejected by toxic effect on its T-killer cells and NK cells, macrophages, antibodies that cause cytolysis. Pathomorphology organs during transplant rejection using the example of a kidney transplant. Hyperacute rejection: The kidney acquires a flabby consistency, mottled appearance with a cyanotic tint. Microscopically, extensive accumulations of neutrophils are detected along the periphery of the vessels and in the glomeruli; fibrin thrombi and fibrinoid necrosis of the walls of arterioles may be present in the lumen of the vessels. Extensive infarcts form in the renal cortex. Acute rejection: characterized by the formation of vasculitis, interstitial edema and infiltration of mononuclear cells, focal necrosis is formed on the side of the tubules. With severe damage to the arterioles, infarctions and subsequent cortical atrophy can form. Chronic rejection: characterized by interstitial fibrosis, a decrease in the specific proportion of parenchyma due to tubular atrophy. Obliterating fibrosis forms in the arteries of the cortical layer. Possible splitting basement membranes glomerular capillaries. Mononuclear cell infiltrates may be present in the interstitium.