Histamine. Stand out when degranulation fat cells, basophils, to a lesser extent by the endings of sensitive fibers, nervous, muscle and other cells. The formation of gastamine was found after 30 seconds after the interaction of allergen with antibodies, and it reaches its maximum by 1.5 minutes.
Histamine causes the extension of vessels, an increase in their permeability, especially capillaries and Volet. In the stomach there are receptors G2, when interacting with which histamine causes secretion enhancing, and in the smooth muscles of the intestine and the uterus, G1 receptors were detected, when interacting with which histamine leads to a reduction in smooth muscles. In addition, histamine has a chemotaxic effect and attracts to the site allergic reaction Eosinophils, which is explained, probably the presence of histaminate in the granules of eosinophils, causing the inactivation of histamine. This is probably, as well as the presence of a special mediator - the chemotaxis of eosinophil factor - can be explained by eosinophilia under a number of allergic reactions immediate type.
Serotonin. It is formed in the degranulation of fat cells and platelets and has a predominantly vascular effect in the form of an increase in permeability. In person, serotonin as a mediator does not take part in the formation of instant allergic reactions. It has been proven only in experimental animals ( guinea pigs, rats, rabbits, dogs).
Leukotrienes in 4, d 4 are formed from phospholipids membranes of fat cells and PM leukocytes. Causes a slow and long-term reduction in smooth muscles, bronchi, intestines, uterus. The effect of this mediator is not removed by antihistamine preparations and proteolytic enzymes. When interacting with allergic antibodies, allergen histamine is released after 1 -2 min, and leukotrienes - after 16-32 minutes.
Bradykinin. It is a polypeptide formed as a result of complex transformations of blood proteins. It sharply increases the permeability of the vessels, rather than histamine, expands capillaries, arratery, causes pain, decline arterial pressure, increases exudation and leukocyte emigration, strengthens the reduction of smooth muscles. Last effect It is formed slower than under the action of histamine and acetylcholine.
Acetylcholine. It is formed in the synapses of cholinergic nerves, and as a result of a decrease in the activity of cholinesterase, its content in the blood at an immediate type of allergies increases. Acetylcholine causes the extension of blood vessels and an increase in their permeability, reducing smooth muscles. It is also believed that allergen, acting on the tissue of the sensitized organism, causes the transition of associated acetylcholine to the free one.
Prostaglandins. First obtained from men's sex glands. They are derivatives of arachidonic acid. About 20 different prostaglandins are known. Prostaglandins E1 and E 2 inhibit the liberation of MRS, contributing to these relaxation of smooth muscle bodies, and strengthen the formation of the CAMF in the fat cells, which improves the cell power supply and inhibits the degranulation and, thus, the release of immediate allergies. Prostaglandin E 2 stimulates the exemption from the fat cells of histamine, leukotrienes and other mediators. It is important to influence them on the smooth muscles of the bronchi. Constrictor influences of Prostaglandin E 2 and the Dlyative Effect E 1 are shown. They have the same effect on the vessels.
Another possible mediators of allergic reactions is peptide P, or an Euler substance.
Peptide P extends Peri - Feric vessels, providing a hypotensive effect, causes a reduction in smooth muscles gastrointestinal tract. The last effect is not removed antihistamine drugs, atropine and adrenolytic substances. Thus, analyzing
the biological activity of the mediators of immediate allergies, it is necessary to note their pronounced vascular effect (extension of vessels, increase their permeability), reduction of smooth muscles and chemotaxic effects for eosinophils, pain. The main mediators of instant allergies are presented in Table 7.3.
Basic mediators immediate allergies
Table 7.3.
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Types of allergic reactions (hypersensitivity reactions). Hypersensitivity immediate and slow-type. Stages of allergic reactions. Step-by-step mechanism for the development of allergic reactions.
1. 4 types of allergic reactions (hypersensitivity reactions).
Currently, on the mechanism of development, 4 types of allergic reactions (hypersensitivity) are accepted. All these types of allergic reactions are usually rarely found in pure form, more often they coexist in different combinations Or go from one type of reaction to another type.
At the same time, the I, II and III types are due to antibodies, are and relate to immediate type hypersensitivity reactions (GNT). The reactions of the type IV type are due to sensitized T cells and belong to slow-type hypersensitivity reactions (GZT).
Note!!! - This is a reaction of hypersensitivity, launched by immunological mechanisms. Currently, all 4 types of response are considered to be hypersensitivity reactions. However, under true allergies Understand only such pathological immune reactions that proceed by the mechanism of atopy, i.e. According to I, the reactions II, III and IV types (cytotoxic, immunocomplex and cellular) types are referred to autoimmune pathology.
- First Type (I) - Atopic, anaphylactic or reacting type - due to antibodies of the IGE class. When allergen interacts with IgE fixed on the surface of the fat cells, these cells are activated and the release of deposited and newly formed allergy mediators followed by the development of an allergic reaction. Examples of such reactions - anaphylactic shock, otkinke, polynosis, bronchial asthma, etc.
- Second Type (II) - Citotoxic. In this type of allergens becomes their own cells of the body, the membrane of which acquired the properties of autoallergens. This occurs mainly when they are damaged as a result of the effects of drugs, enzymes of bacteria or viruses, as a result of which the cells change and perceived by the immune system as antigens. In any case, for the occurrence of this type of allergies, antigenic structures Must acquire properties of autoantigen. The cytotoxic type is caused by IgG- or IgM, which are directed against the hypers located on the modified cells of the organism of their own tissues. The binding of AT with AG on the surface of the cell leads to an integration of the complement, which causes damage and destruction of cells, subsequent phagocytosis and removing them. The process also involve leukocytes and cytotoxic lymphocytes. Binding to IgG, they are involved in the formation of antibody-dependent cell cytotoxicity. It is by cytotoxic type that autoimmune hemolytic anemia is developed, medicinal allergies, autoimmune thyroiditis.
- Third Type (III) - Immunokomplexin which the tissues of the body are damaged by circulating immune complexes with the participation of IgG- or Igm having a large molecular weight. So With III type, the reactions are due to II, the IGG and IGM. But in contrast to type II, with an allergic reaction of the type III, the antibody interacts with soluble antigens, and not with the cells on the surface of the cells. The resulting immune complexes are circulated in the body and are fixed in the capillaries of various tissues, where the complement system activates, causing the flow of leukocytes, the release of histamine, serotonin, lysosomal enzymes, damaging endothelium vessels and tissues in which the immune complex is fixed. This type of reaction is essential for serum diseases, medicinal and food allergies, with some auto alicle diseases (SLE, rheumatoid arthritis and etc).
- Fourth (IV) type of reactions - slow-type hypersensitivity or cell-indirect hypersensitivity. Slow-type reactions are developing in a sensitized organism 24-48 hours after contact with an allergen. With IV type of reaction, the role of antibodies is performed by sensitized lymphocytes. AG, contacting with ag-specific receptors on T cells, leads to an increase in the amount of this population of lymphocytes and their activation with the release of mediators of cellular immunity - inflammatory cytokines. Cytokines cause clusters of macrophages and other lymphocytes, involve them in the process of destruction of the ag, resulting in inflammation. Clinically, this is manifested by the development of hypergic inflammation: cell infiltrate is formed, the cell basis of which is mononuclears - lymphocytes and monocytes. The cellular type of reaction underlies the development of viral and bacterial infections (Contact dermatitis, tuberculosis, myoses, syphilis, lepring, brucellosis), some forms of infectious allergic bronchial asthma, reaction of transplant and antitumor immunity reactions.
| Type of reaction | Development mechanism | Clinical manifestations | ||
| Type I Reactive Reactions | Develops as a result of allergen binding with IgE fixed on fat cells, which leads to emission from allergy mediators cells, which cause clinical manifestations | Anaphylactic shock, Otka Quince, Atopic Bronchial Asthma, Polynosa, Conjunctivitis, Urthius, atopic dermatitis, dr. | ||
| Type II Cytotoxic Reactions | Conditioned IgG or IgM, which are directed against the hypers located on cells of their own tissues. Complement activation occurs, which causes cytolysis of target cells | Autoimmune hemolytic anemia, thrombocytopenia, autoimmune thyroiditis, medicinal agranulocytosis, etc. | ||
| Type III Immunocomplex reactions mediated by immune complexes | Circulating immune complexes with IgG or Igm are fixed to the capillary wall, activate the complement system, tissue infiltration by leukocytes, their activation and products of cytotoxic and inflammatory factors (histamine, lysosomal enzymes, etc.), damaging endothelium vessels and tissues. | Serum disease, medicinal and food allergies, SLE, rheumatoid arthritis allergic Alveolit, necrotic vasculitis, etc. | ||
| Type IV cell-indirect reactions | Sensitized lymphocytesBy contacting the hypertension, the inflammatory cytokines produce, which activate macrophages, monocytes, lymphocytes and damage the surrounding tissues, forming cell infiltrate. | Contact dermatitis, tuberculosis, mycoses, syphilis, lepring, brucellosis, reaction of transplant rejection and antitumor immunity. |
2. Hypersensitivity of immediate and slow-type type.
What is the principal difference between all these 4 types of allergic reactions?
And the difference in how mainly the type of immunity, is humoral or cellular, is caused by these reactions. Depending on this distinguish:
3. Stages of allergic reactions.
In most patients, allergic manifestations are due to IGE-class antibodies, therefore we will consider the mechanism for the development of allergies on the example of the allergic reaction of type I (ATOPIA). In their current, three stages are distinguished:
- Immunological stage - includes changes in the immune system occurring during the first contact of allergen with the body and the formation of the corresponding antibodies, i.e. Sensibilization. If by the time of the formation of AT allergen removed from the body, no allergic manifestations Not coming. If the allergen arrives again or continues to be in the body, the Allergen - Antibody complex is formed.
- Patochimical - Emission of biologically active allergy mediators.
- Pathophysiological - Stage of clinical manifestations.
This separation at the stage is sufficiently conditionally. However, if you imagine the process of development of allergies step by step, It will look like this:
- First contact with allergen
- Education IgE.
- IgE fixation on the surface of the fat cells
- Sensitization of the body
- Repeated contact with the same allergen and the formation of immune complexes on the membrane of fat cells
- Exit of mediators from fat cells
- Action of mediators on organs and fabrics
- Allergic reaction.
Thus, the immunological stage includes paragraphs 1 - 5, Patochimic - paragraph 6, Pathophysiological - paragraphs 7 and 8.
4. Step-by-step mechanism for the development of allergic reactions.
- First contact with an allergen.
- Education IG E.
At this stage of development, allergic reactions resemble a normal immune response, and are also accompanied by the production and accumulation of specific antibodies that can be connected only with the allergen that caused their education.
But in the case of atopy, it is an education for the allergen that IGE received, and in increased quantities In relation to other grades of immunoglobulins, therefore it is also called IG -E dependent allergies. IgE are produced locally, mainly in the submucosal shell of fabrics in contact with external environment: in respiratory tract, skin, gastrointestinal tract. - IgE fixation to the membrane of fat cells.
If all other immunoglobulin classes after their formation are freely circulated in the blood, then the IgE has a property immediately attached to the puffy cell membrane. Fat cells are immune cells connective tissue that are located in all tissues in contact with the external environment: the tissue of the respiratory tract, the gastrointestinal tract, as well as the connecting fabrics surrounding blood vessels. These cells contain such biologically active substances as histamine, serotonin, etc., and are called mediators of allergic reactions. They possess pronounced activity And there are a number of effects on the fabrics and organs, causing allergic symptoms. - Sensitization of the body.
For the development of allergies, one condition is required - preliminary sensitization of the body, i.e. The emergence of increased sensitivity to alien substances is allergens. Increased sensitivity to this substance is formed at the first meeting with it.
Time from the first contact with the allergen to the occurrence of increased sensitivity to it is called a period of sensitization. It can range from several days to several months or even years. This period, during which an IGE is accumulated in the body, fixed to the basophils and fat cells membrane.
The sensitized organism is the one in which the stock of antibodies or T-lymphocytes (in the case of GZT) sensitized to this particular antigen.
Sensitization is never accompanied by clinical manifestations of allergies, because during this period only AT is accumulated. Immune complexes AG + AD have not yet been formed. The same fabric, causing allergies, are capable of not single AT, but only immune complexes. - Repeated contact with the same allergen and the formation of immune complexes on the membrane of the fat cells.
Allergic reactions occur only when re-encountered a sensitized organism with this allergen. Allergen binding occurs with already ready-made AT on the surface of the fat cells and the formation of immune complexes: allergen + at. - The output of mediators of allergy from fat cells.
Immune complexes damage the membrane of fat cells, and allergy mediators come into the intercellular medium. Fabrics rich in fat cells (leather vessels, serous shells, connective tissue And others) are damaged by the released mediators.
With long-term exposure of allergens, the immune system uses additional cells to reflect the intrusion of the antigen. A more row is formed chemical substances - mediators, which causes further discomfort suffering allergies and increases the severity of symptoms. At the same time, the mechanisms of inactivation of allergy mediators are oppressed. - The effect of mediators on organs and fabrics.
The effect of mediators determine the clinical manifestations of allergies. System effects are developing - expanding blood vessels and an increase in their permeability, mucous secretion, nervous stimulation, smooth muscle spasms. - Clinical manifestations of an allergic reaction.
Depending on the body, the type of allergens, the path of income, the place where the allergic process is played, the effects of a mediator of allergies, symptoms may be system-wide (classical anaphylaxis) or localized in separate systems of the body (asthma - in respiratory tract, eczema - in the skin ).
Itching, runny nose, tear, ethnic, shortness of breath, falling pressure, etc. and develops the corresponding picture allergic rhinitis, conjunctivitis, dermatitis, bronchial asthma or anaphylaxia.
In contrast to the above-described hypersensitivity of the immediate type, a slow-type allergy is caused by sensitized T cells, and not antibodies. And those cells of the organism are destroyed with it, on which the immune complex of the AG + sensitized T-lymphocyte occurred.
Reduction in the text.
- Antigens - AG;
- Antibodies - at;
- Antibodies \u003d the same as immunoglobulins (AT \u003d Ig).
- Slow-type hypersensitivity - GZT
- Immediate type hypersensitivity - GNT
- Immunoglobulin A - IGA
- Immunoglobulin G - IgG
- Immunoglobulin M - IGM
- Immunoglobulin E - IGE.
- Immunoglobulins - Ig;
- Antigen reaction with antibody - AG + AT
| Mediator | Effect |
| Migration inhibiting factor | Macrophage migration braking, phagocytosis enhancing, granuloma formation |
| Transfer factor | Passive transfer of hypersensitivity |
| Lymphotoxin | Lisace target cells |
| Chemotaxis macrophage factors, monocytes | Chemotaxis macrophages, monocytes |
| Proliferation inhibiting factor | Limphocyte proliferation braking |
| Skin reactivity factor | Causes inflammation at the injection site |
| Interferons (α, β, γ) | Activates T-lymphocytes killers, inhibits cell infection with a virus |
| Mitogenic factors (IL-2, IL-3, IL-6) | Blast transformation of lymphocytes |
Lymphotoxin. The person has a molecular weight of 80,000. Probably, this polypeptide has a cytotoxic effect, causing the destruction of target cells containing antigen and braking of the regeneration of these cells.
Skin reactivity factor. Enhances the permeability of the vessels, the expansion of them, which is manifested by redness and sealing section of the slow-type hypersensitivity. The skin reactivity factor is albumin, probably in a complex with fatty acids.
All these mediators have a cytotoxic effect, cause cell alteration, and also stimulate migration from the blood of lymphocytes, macrophages. That is why the slow-type hypersensitivity is characterized by mononuclear infiltration.
Pathophysiological stage of allergies
The pathophysiological stage of allergic reactions is a complex of functional, biochemical and structural changes On cellular, fabric, organic and organized levels arising from immunological shifts and isolating mediators of allergies in the interaction of allergens with a material substrate sensitization.
In this stage, for any allergic processes of an immediate type, especially anaphylactic shock, the most characteristic violations from cardiovascular, respiratory, digestive, endocrine, nervous systems, blood circulation systems, metabolism. System shifts are a consequence of mediators of mediators causing microcirculation disorders (increasing permeability, expansion of capillaries, violation of the rheological properties of blood), spasm of a smooth muscles of bronchi and other smooth muscle bodies (intestines, uterus, etc.), increasing the secretion of glucocorticoids and catecholamines, changes in the processes of excitation and Brakes at various levels nervous systemleading to the constraints of the central regulation of vital functions.
Local manifestations in allergic reactions are characterized by cell alteration, the development of edema, inflammatory phenomena, cytotoxic and cytolytic effect.
Depending on the predominance of general or local manifestations, allergic reactions are divided into systemic and local. The systemic reactions of immediate-type include anaphylactic shock, serum disease, urticaria; Local - the phenomenon of Ardus - Sakharov, the phenomenon of Ovei, Polyindoza, bronchospasm.
For the stage of pathophysiological changes in slow motion allergies, the development is characterized inflammatory reaction In the affected organs with the presence of mononuclear infiltration consisting of lymphocytes, monocytes, macrophages. Infiltrating cells have mainly hematogenic origins. Alteration and lysis of cells and tissues in the focus of inflammation are largely determined by the effects of cellular immunity mediators, in particular, the cytotoxic effect of sensitized lymphocytes.
The local allergic reactions of the delayed type include tuberculin, contact dermatitis, most organosophic autoimmune processes, transplant rejection; to systemic diseases Collagenoses belong.
The mechanisms of autoallergia
Immunological tolerance means recognition of antigens of its own organism (autoantigen) and, as a result, the absence of immunity reaction.
With the abolition of the tolerance caused by the action to the body of various damaging factors, autoimmune diseases occur, in the pathogenesis of which the humoral or cellular immunity (antibodies or T-lymphocytes) is played. It is believed that the immune system can form an immune response against any autoantignen.
Two main groups of autoimmune processes are distinguished: organospecific (myasthenia, thyroiditis hashimoto, thyrotoxicosis with diffuse goiter) and systemic (rheumatoid arthritis, systemic red lupus, etc.)
Among the many representations of pathogenesis of autoallergia, two main groups of hypotheses can be distinguished, which are based on various mechanisms:
1 - the normal immune system naturally reacts to the modified (modified) influenced by various influences (chemical, physical, infectious, etc.) of antigens of own tissues (secondary endo allergens);
2 - The defective immune system reacts against normal tissue antigens.
In the case of autoamelergia, in accordance with the first mechanism, the causal chain is as follows: the occurrence of a modified tissue antigen ^ Normal immunological response in the form of developing antibodies or sensitized lymphocytes ^ Their destructive effect on cells and tissues. IN last years This view caused a number of objections and critical comments (R.V. Petrov). First of all, in accordance with the point of view R.V. Petrova (see above), modified tissue antigens should not be attributed to endoallergens, and to a special species of exoallergens, therefore, developing on this basis, the process is not autoimmune (auto allergic). Moreover, the interaction of antibodies and sensitized lymphocytes with a modified antigen can be viewed as a protective reaction, since it should entail the destruction of such an antigen, its removal from the body and the rapid self-esteem, which is not typical for autoimmune diseaseswhich are self-sustaining chronic character.
In addition, there is no interpretation of the estimated damage to the antibodies of normal tissues in accordance with this theory, since antibodies are produced against modified antigens and, by virtue of its specificity, cannot interact with normal antigens. All subsequent concepts of autoamellergia proceed from the fundamental ideas that any autoimmune disorders are diseases immune system the body from where it follows the almost important conclusion that for effective struggle They are necessary, first of all, the correction of immunological mechanisms, and not affected by tissues. In particular, F. Bernet proposed a hypothesis, according to which the initial violation of the autoimmune reactions is the primary violation of the immunity system and immunological mechanisms, which leads to the appearance of a prohibited clone of cells, which interacts with normal tissue and organ antigens, causing them damage. In this case, the pathogenesis of autoimmune diseases seems to be as follows: violation of the genome of lymphocyte ^ accumulation of the prohibited clone of cells ^ immune response of the cells of the prohibited clone with the advent of autoantibodies or sensitized lymphocytes, which interact with normal tissue antigens, causing their alteration. This hypothesis attracts the attention of researchers because explains the self-sustaining nature of autoimmune processes and the feasibility of using immunosuppressants. In addition, it allows you to conclude that infectious (bacterial and viral) agents in the presence of a hereditary predisposition to autoimmune processes can cause mutations in T- and variables, which leads to the appearance of a prohibited clone of cells.
In the heart of autoimmune processes, there may be lack of immunological tolerance to a number of antigens of "barriers". Therefore, with damage to histohematic barriers and impaired physiological isolation of the antigens of these organs, they can flow into the bloodstream, causing the activation of the V- and T-system of immunity, the formation of antibodies or sensitized lymphocytes, which damage normal organs and fabric. Proof of the vitality of such a presentation is the modeling of autoimmune defeats of the kidneys, the brain, the semennikov, when introduced into the body of cells and the extracts of organs (kidney, brain, heart), together with the Freound filler.
In some cases, the development of autoimmune processes explain the presence of cross-reactive antigens (for example, streptococcus and heart muscle). Streptococcus includes immuno-poets in cells producing antibodies that interact with streptococcus and simultaneously with similar determinants of tissue antigens.
A series of hypotheses considers autoimmune reactions as immunodeficient states. So, X. FUIDADBERG believes that if there are genes in the body of a weak and strong immunological response in the body, some infectious pathogens can be long in the tissues, leading to their destruction, and antigens damaged cellsBy entering blood, they can cause a strong immunological response that ultimately will lead to autoimmune damage to normal tissues.
According to R.V. Petrova, this hypothesis questioned the use of immunosuppressants in some cases, including hormonal, and draws attention to the feasibility of developing stimulation of genes of a weak immunological response. In addition, this hypothesis binds the development of autoimmune processes with chronic infectionsFor example, Streptococco.
Some researchers explain the development of autoimmune reactions to the immunodeficiency - the insufficiency of the suppressor function of T-lymphocytes, which ultimately leads to the activation of an auto-aggressive clone of cells capable of causing an autoimmune reaction with normal tissue antigens. The deficit of suppressors can be explained in congenital underdevelopment of thymus or the effect of infection, especially viral. In recent years, (X. Cantor) has been found that before the development of acute sclerosis and rheumatoid arthritis, T-lymphocytes suppressors disappear from blood and tissue.
Clinical observations show that with such classical autoimmune processes, as a systemic red lupus, rheumatoid arthritis, multiple sclerosisThere is a deficit of transsers. Finally, the basis of autoimmune processes lie violations normal processes Recognition. Lymphocytes have receptors that ensure the recognition of "their" antigens. The blockade of these receptors using anti-receptor antibodies leads to cancellation of tolerance to its own components of the body and the appearance of an aggressive clone immunocompetent cells, for example, insulin resistant form sugar diabetes It is explained by the accumulation of autoantibodes against cell receptors, normally interacting with insulin.
General Principles of Diagnostics Sensitization
The diagnosis of enhanced sensitivity is necessary to prevent the development of allergic reactions. For this purpose, a series of samples are carried out with the introduction of the alleged allergen (intracodently, conjunctivative, intranasally, in the respiratory tract). However, cases of shock reactions are noted in response to scarification or even intradermal sample. In addition, such samples do not always allow us to find out increased sensitivityFor even negative intradermal samples before use, for example, antibiotics and other medicinal substances Do not exclude the possibility of developing anaphylactic shock and death of the patient (V.A. Fradkin).
Considering the insecurity of diagnostic samples, a number of express methods for diagnosing sensitization have been developed. This is an indicator of damage to the neutrophils according to the refrigerant, the reaction of the agglomeration of leukocytes and the indirect degranulation of basophils according to Shelly, the reaction of blast-transformation of leukocytes, degranulation of fat cells, etc. However, the remark V.A. Frakdina that the above-mentioned methods of diagnosing sensitization require a lot of time to obtain results, while appointment and administration medicinesIn relation to which hypersensitivity is possible, it is required to be carried out. Therefore, the most simple and reliable methods for diagnosing sensitization are being conducted, allowing them to apply them in any medical institution.
There are two main class of chemical mediators responsible for the reactions of the hypersensitivity of the immediate type. Essential, or primary, mediators are molecules that are already accumulated in the granules of fat cells and basic philates and begin to secrete into the estaellular medium immediately after contacting the cell with the antigen. These mediators are represented
four main molecules forms: 1) with vasoactive amines - histamine, serotonin, 2) chemotactic factors for granulocytes, 3) enzymes, 4) proteoglycans - heparin (in fat cells) and chondroitin sulfate (in basophils). Secondary mediators are molecules synthesized by DE NOVO after contacting the fat cells, baeophiles, or other antigen inflammation cells. Mostly, secondary mediators are represented by lipid derivatives and include leucotrienes and a factor activating platelets.
Targets of one of the main mediators allergic lesions - Histamine - are smooth muscles, blood vessels, some ecocrine glandsleukocytes. Events leading to development various shapes Allergic reactions are developing in several stages (Fig. 16.1). The body susceptible to allergies is already sensitized by specific IGE antibodies, obese cells. Pre-sensitization passed during primary contact with the allergen and did not have consequences in the form of the development of the reaction state. The same allergen during re-penetration into the body interacts with the ESGE preexisting. Cross coupling
Fig. 16.1. Participation of the pcttashna in YallerppsCC reactions.
As a result of the interaction of allergen with specific IgE-antibodies, pre-existing on fat cells, the active emission of histamine from the granules begins. Histamine, interacting with receptors on smooth muscles and / or cells vascular endotheliumimplements its pathogenetic action
allergen allergen with IgE provides the intake of CAA + inside the cell, as a result of which the cell is activated and histamine is released from intracellular granules. The mediator interacts with the appropriate H1 and H2 receptors presented on target cells. The main manifestation of the pathogenetic action of histamine is a sharp reduction in the smooth muscles. Such a reduction is responsible, in particular, for bronchospasm during asthma or anaphylactic shock. Histamine influence on vascular system Manifested mainly in the defeat of epithelial cells. They narrow under the action of histamine, exposing the vascular wall, which contributes to the increased permeability of large molecules into the out-of-rise area.
The pathogenetic effect on the body similar to the histamine has another mediator - serotonin. In humans, the activity of this compound is observed only in terms of platelets and cells of the small intestine.
Chemotactic factors, wrapped from granules of fat cells, provide the influx of granulocytes and neutrophils into the focus of the development of the reaction.
Allergy mediators are released or synthesized when the complexes are allergen-sensitized T-lymphocyte or allergen antibody. These substances play a crucial role in the occurrence of hypersensitivity to one or another irritant.
Mediators of allergic reactions have a vasoactive, precision, chemotactic action, capable of damaging the body tissues and activate the reparation processes. The actions of these substances depend on the type of allergies, the mechanisms of its occurrence, the form of an irritant agent.
Allergy classification
Depending on the severity and speed of the appearance of symptoms after the repeated effects of the irritating agent, the hypersensitivity reaction is divided into 2 groups:
- immediate type reactions;
- slow-type reactions.
The reactions of the hypersensitivity of the immediate type occur almost immediately after repeated exposure irritant. Antibodies formed during the first contact in the allergen are freely circulated in liquid media. In the case of the next penetration of the stimulus, the antigen antibody complex is quickly formed, which causes the rapid occurrence of allergy symptoms.
The development of a slow allergic reaction occurs after 1-2 day after interaction with an irritant agent.
This reaction is not related to the production of antibodies - sensitized lymphocytes are involved in its development. The slow development of the response to the impact of the irritant is due to the fact that for the accumulation of lymphocytes in the inflammation area, more time is required, compared with the immediate response of hypersensitivity, which is characterized by the formation of the antigen antibody complex.
Immediate type hypersensitivity mediators
With the development of an immediate response of hypersensitivity, the role of target cells is performed by labrocytes, or fat cells and basophilic leukocytes, which have F-receptors to immunoglobulin E and immunoglobulin G. After connecting the antigen with antibodies, degranulation occurs and mediators are released.
Mediators of allergic reactions of instant type are as follows: 
- histamine refers to the main allergy mediators. It suppresses T cells, their reproduction, the differentiation of B-cells and the production of antibodies by plasmacites, activates the activities of T-suppressors, has a chemotaxic and chemokinetic effect against eosinophils and neutrophils, reduces the process of separation of lysosomal enzymes with neutrophils.
- serotonin increases vessel spasm of the most important organs, such as heart, lungs, kidneys, brain. Under its influence there is a reduction in the smooth muscles. Serotonin does not have an anti-inflammatory effect characteristic of histamine. This mediator activates T-suppressors milk gland and spleen, as well as migration of T-cells of the spleen in bone marrow and the lymph nodes. In addition to immunosuppressing action, serotonin is also able to stimulate immunity. Under the influence of the mediator, the sensitivity of mononuclears to a variety of chemotaxic factors increases.
- bradykin is an element of a kinin system. This mediator contributes to the expansion and increase in the permeability of the vessels, provokes long-lasting bronchospasm, irritatingly affects pain receptors, activates the development of mucus in digestive tract and respiratory tract. Bradykin is rapidly produced in damage to the body tissues, as a result of which many effects characteristic of inflammatory process - vasodilatation, extravagation of plasma, increase in the permeability of vessels, cell migration, painful feelings And hyperalgesia.
- heparin is a mediator from a group of proteoglycans. Heparin has an anticoagulant effect, participates in cell proliferation, contributes to the migration of endothelium cells, reduces the complementary effect, stimulates phago and pinocytosis.
- complement fragments - inflammation mediators. Under their influence, smooth muscles are reduced, histamine is released from the fat cells, that is, an anaphylaxis reaction is developing.
- prostaglandins - B. human organism Prostaglandins E, F, D. Prostaglandins f contribute to the occurrence of heavy attack of bronchospasm. Prostaglandins E, on the contrary, they have an armored effect. Exogenous prostaglandins are able to activate or reduce the process of inflammation, the vessels are expanded under their impact, their permeability increases, the body temperature increases and erythema is developing.
Slow-type hypersensitivity mediators
Lymphokins synthesized by T-lymphocytes are mediators of delayed type allergic reactions. Under their influence in the place of exposure to the stimulus, cell elements are concentrated, infiltration and inflammation process develops.
The skin-reactive factor increases the vascular permeability and accelerates the migration of white blood cells.
A permeability factor has a similar effect. Under the influence of chemotaxis factor in the reaction of hypersensitivity, unsensitized lymphocytes, neutrophils, monocytes, eosinophils are involved. Under the influence of a factor inhibiting migration in the field of inflammation, macrophages are delayed and accumulated. Under the influence of the transfer factor, activity is transferred to nonsensey-protected T-cells. The lymphocytes synthesize interferon, which has antiviral properties, and also activates the function of natural T-killers. The impact of mediators limit the opposing systems to protect target cells.
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