Allergic reactions of the delayed type are examples. Allergic reactions of immediate and delayed type

A delayed-type allergy makes itself felt after a few hours and a day.

When an irritant influences the body, various negative changes occur. They can be expressed directly when the allergen enters, and also be detected after some time. Changes that are delayed are called delayed-type allergic reactions. They may appear in a few hours or days.

What influences the reaction

allergic reactions delayed type begin with the process of sensitization

Delayed allergy occurs in the same way as other reactions. When an irritant enters the body, a process of sensitization occurs. This causes the development of sensitivity of the immune system to foreign substances. The lymph nodes begin to produce pyroninophilic cells. They become "material" for the creation of immune lymphocytes that carry antibodies. As a result of this process, antibodies appear both in the blood and in other tissues, mucous membranes, and body systems.
If re-penetration of the irritant occurs, then the antibodies respond to the allergens, which leads to tissue damage.
How the antibodies that cause delayed-type allergic reactions are formed is not yet fully known. But the fact has been revealed that it is possible to transfer a delayed allergy only with the use of a cell suspension. This mechanism was developed by scientists as a result of an experiment on animals.
If blood serum is used, then it is impossible to transfer antibodies. This is due to the fact that it is necessary to add a certain number of elements of other cells. Lymphocytes play a special role in the formation of consequences.

Characteristics

Delayed-type reactions differ from immediate manifestations in characteristic features.

If signs of damage occur, from the moment the allergen enters the human body until symptoms are detected, it takes from 1 to 2 days.

If you conduct a blood test to identify the allergen, then in the case of delayed manifestations of allergy, antibodies are not detected.

The mechanism of transferring an allergic reaction to a healthy person can only occur when using leukocytes, lymphatic cells and exudate cells. If blood serum is used, the transfer of immediate manifestations will be carried out.

With delayed reactions, sensitized leukocytes can feel the cytotoxic and lytic effects of the stimulus.

In the event of a delayed reaction to tissues, an allergen of a toxic nature is exposed.

The mechanism of the reaction

The process of occurrence of a delayed-type reaction consists of three stages:

immunological;

pathochemical;

pathophysiological.

At the first stage, the thymus-dependent immune system is activated. Strengthening of cellular immune defense occurs with insufficient work of humoral mechanisms:

when the antigen is inside the cell;

when converting cells into antigens.

In this case, the antigens are:

• protozoa;

  mushrooms with spores.

Allergic reactions of a delayed type can occur upon tactile contact with an allergen.

The same mechanism is activated when creating a complex allergen characteristic of contact dermatitis (due to drug, chemical and household irritation).
At the pathochemical stage, the mechanism for the formation of lymphokines, macromolecular substances produced by the interaction of T and B lymphocytes with irritants, is turned on. Lymphokines can be formed depending on:

genotypic features of lymphocytes;

type of antigens;

antigen concentrations.

Lymphokines that affect the formation of a delayed-type reaction can be in the form of:

a factor that inhibits the migration of macrophages;

interleukins;

chemotactic factors;

lymphotoxins;

interferons;

transfer factors.

Also, an allergic reaction is caused by lysosomal enzymes, activation of the kallikrein-kinin system.
At the pathophysiological stage, the mechanism of damage can be expressed in the form of three reactions.

During the direct cytotoxic action of sensitized T-lymphocytes, the allergen is recognized by the lymphocyte, and they come into contact with each other. At the stage of a lethal blow, the damage mechanism is activated. The defeat occurs at the third stage of target cell lysis, when its membranes disintegrate, mitochondria swell.

Under the action of T-lymphocytes through lymphotoxin, only those cells that caused its occurrence or triggered the mechanism of its production are damaged. In this case, the cell membrane begins to collapse.

When lysosomal enzymes are released during phagocytosis, tissue structures are damaged. The mechanism of enzyme formation begins in macrophages.

Basic distinctive feature delayed thyra reactions is an inflammatory process. It is formed in various organs, which leads to the occurrence of diseases of the body systems.

Inflammation with the formation of granulomas can be caused by exposure to:

bacteria;

fungal spores;

pathogenic and conditionally pathogenic microorganisms;

substances with a simple chemical composition;

• inflammatory processes.

Types of delayed reactions

There are enough delayed reactions a large number of. The main common occurrences are:

bacterial allergy;

contact allergy;

autoallergy;

homograft rejection reaction.

bacterial allergy

A delayed bacterial lesion is often detected with the introduction of various vaccines, as well as diseases of an infectious nature. These include:

In the event of sensitization and the introduction of an allergen, the reaction occurs no earlier than 7 hours after the irritant enters the body. A person may experience redness, the skin may thicken. In some cases, necrosis appears.
If carried out histological examination, then bacterial allergy is characterized by mononuclear infiltration.
In medicine, delayed-action reactions are widely used in the determination of various diseases (Pirquet, Mantoux, Burne reactions). Apart from skin, symptoms are evaluated on the cornea of ​​the eye, bronchi.

contact allergy

With contact allergies, manifested in the form of dermatitis, the effect on the body occurs with the help of low molecular weight substances:

dinitrochlorobenzene;

picrylic acid;

There is also the influence of ursol, platinum compounds, components cosmetics. When they enter the body, these incomplete antigens combine with proteins and cause an allergic reaction. The better the substance combines with the protein, the more allergenic it is.
The most pronounced symptoms occur after 2 days. The reaction is expressed as a mononuclear infiltration of the epidermis. As a result of tissue degeneration, structural disturbance, epidermis exfoliation occurs. This is how the allergy is formed.

Autoallergy

Delayed allergens can cause serious damage

Sometimes allergens are formed directly in the body. They affect cells and tissues, causing severe damage.
Endoallergens - one of the types of autoallergens, are present in the body of every person. When separating some tissues from the apparatus of immunogenesis, immunocompetent cells perceive these tissues as foreign. Therefore, they affect the process of producing antibodies.
In some cases, autoallergens are purchased. This is due to protein damage. external factors(cold, hot).
If a person's own antigens combine with bacterial allergens, then the formation of infectious autoallergens is detected.

Homograft rejection

When transplanting tissues, complete tissue engraftment can be observed when:

autotransplantation;

homotransplantation in identical twins.

In other situations, rejection of tissues and organs occurs. This process is caused by a reaction of an allergic type of delayed action. 1–2 weeks after transplantation or tissue rejection, the body responds to the introduction of donor tissue antigens under the skin.
The reaction mechanism is determined by lymphoid cells. If tissue transplantation was carried out in an organ with a weak lymphatic system, then the tissue is destroyed more slowly. When lymphocytosis occurs, we can talk about the beginning rejection.
When a foreign tissue is transplanted, the recipient's lymphocytes become sensitized. Soon they pass into the transplanted organ. Their destruction occurs, the release of antibodies, violation of the integrity of the transplanted tissue.
Delayed type reactions can be expressed as various signs. They require increased diagnosis and careful treatment, as they become the causes of serious illnesses.

Allergy is pathological condition, in which the human body perceives some substances that do not pose a danger as foreign agents. A hypersensitivity reaction develops, which is associated with the formation of immune complexes. Depending on the pathogenesis of development, allergic reactions of the immediate type and delayed are distinguished.

Delayed-type allergic reactions develop over time and do not carry the same danger as immediate-type reactions. The latter appear within a few minutes after exposure to the allergen. They cause serious harm to the body and, if left untreated, can be fatal.

Causes of the development of allergic reactions of the immediate type

An allergy develops when the body comes into contact with any substance to which there is hypersensitivity. For humans, this substance is not dangerous, but the immune system for unexplained reasons, believes otherwise. The most common allergens are:

• dust particles;
• some medicines;
• plant pollen and mold fungi;
• highly allergenic foods (sesame, nuts, seafood, honey, citrus fruits, cereals, milk, beans, eggs);
• poison of bees and wasps (with a bite);
• animal hair;
• artificial fabrics;
• household chemical products.

The pathogenesis of the development of an allergy of the immediate type

When the allergen first enters the body, sensitization develops. For unknown reasons, the immune system concludes that this substance is dangerous. In this case, antibodies are produced that gradually destroy the incoming substance. When the allergen enters the body again, the immune system is already familiar with it. Now he immediately puts into play the antibodies developed earlier, thereby causing an allergy.

An allergic reaction of the immediate type develops within 15-20 minutes after the intake of the allergen. It takes place in the body in three stages, going sequentially one after another:

1. immunological reaction. The incoming antigen interacts with the antibody. This is immunoglobulin E, which is attached to mast cells. In the granules of the cytoplasm of mast cells are mediators of allergic reactions of the immediate type: histamines, serotonins, bradykinins and other substances.
2. pathochemical reaction. It is characterized by the release of allergy mediators from mast cell granules.
3. pathophysiological response. Mediators of an immediate allergic reaction act on body tissues, causing an acute inflammatory response.

What are immediate allergic reactions?

Depending on which organ or tissue the allergen has entered, various reactions develop. Immediate type allergies include urticaria, angioedema, atopic bronchial asthma, allergic vasomotor rhinitis, anaphylactic shock.

Hives

Acute urticaria is characterized by the sudden onset of an itchy, blistering rash. The elements have a regular rounded shape and can merge with each other, forming elongated blisters. Urticaria is localized on the limbs and trunk, in some cases - on the mucous membrane of the oral cavity and larynx. Usually, elements appear at the site of exposure to the allergen, for example, on the arm, near a bee sting.

The rash lasts for several hours, after which it disappears without a trace. In severe cases, urticaria can last for several days and be accompanied by general malaise and fever.

Hives

Quincke's edema

Quincke's edema is a giant urticaria, which is characterized by a sharp swelling of the subcutaneous fat and mucous membranes. Pathology can affect any part of the body: face, oral cavity, intestines, urinary system and brain. One of the most dangerous manifestations is laryngeal edema. It also swells the lips, cheeks and eyelids. Quincke's edema, affecting the larynx, leads to difficulty in breathing up to complete asphyxia.

This type of immediate allergic reaction usually develops in response to medicinal substances or the venom of bees and wasps.

Quincke's edema

Atopic bronchial asthma

Atopic bronchial asthma is manifested by sudden bronchospasm. Difficulty breathing, paroxysmal cough, wheezing, viscous sputum, cyanosis of the skin and mucous membranes occur. The cause of the pathology is often the inhalation of allergens: dust, pollen, animal hair. This variant of an immediate allergic reaction develops in patients with bronchial asthma or in persons with a hereditary predisposition to this disease.

Allergic vasomotor rhinitis

Pathology, similar to atopic bronchial asthma, develops when allergens are inhaled. Vasomotor rhinitis, like all allergic reactions of the immediate type, begins against the background of complete well-being. The patient develops itching in the nose, frequent sneezing, abundant secretion of rare mucus from the nose. At the same time, the eyes are affected. There is lacrimation, itching and photophobia. In severe cases, an attack of bronchospasm joins.

Anaphylactic shock

Anaphylactic shock is the most severe form of allergy. Its symptoms develop at lightning speed, and without emergency care, the patient dies. Usually the cause of development is the introduction medicines: penicillin, novocaine and some other substances. In young children with hypersensitivity, anaphylactic shock may occur after eating highly allergenic foods (seafood, eggs, citrus fruits).

The reaction develops 15-30 minutes after the allergen enters the body. It is noted that the sooner anaphylactic shock occurs, the worse the prognosis for the patient's life. The first manifestations of the pathology are severe weakness, tinnitus, numbness of the limbs, a tingling sensation in the chest, face, soles and palms. The person turns pale and breaks out in a cold sweat. Falls sharply arterial pressure, the pulse quickens, there is a tingling behind the sternum and a feeling of fear of death.

In addition to the above symptoms, anaphylactic shock may be accompanied by any other allergic manifestations: rashes, rhinorrhea, lacrimation, bronchospasm, Quincke's edema.

Emergency care for immediate type allergies

First of all, with the development of an allergic reaction of an immediate type, it is necessary to stop contact with the allergen. To eliminate hives and vasomotor rhinitis usually enough to take antihistamine. The patient needs to ensure complete rest, apply a compress with ice to the site of the rash. More severe manifestations of an allergy of the immediate type require the introduction of glucocorticoids. With their development, one should call ambulance. Then provide an influx of fresh air, create a calm atmosphere, give the patient warm tea or compote to drink.

Urgent care in anaphylactic shock is the introduction hormonal drugs and pressure normalization. To facilitate breathing, it is necessary to lay the patient on pillows. If respiratory and circulatory arrest is recorded, then cardiopulmonary resuscitation is performed. In a hospital or ambulance, tracheal intubation with oxygen is performed.

Performing cardiopulmonary resuscitation

Cardiopulmonary resuscitation includes chest compressions and mouth-to-mouth artificial respiration. It is necessary to carry out resuscitation in the absence of consciousness, breathing and pulse in the patient. Before the procedure, you should check the patency of the respiratory tract, remove vomit and other foreign bodies.

Cardiopulmonary resuscitation begins with chest compressions. You should fold your hands into the castle and press on the middle of the sternum. In this case, the pressure is carried out not only by the hands, but also by the entire upper body, otherwise there will be no effect. 2 pressures are performed per second.

For artificial respiration, you need to close the patient's nose, throw back his head and blow air strongly into his mouth. To ensure your own safety, you should put a napkin or handkerchief on the lips of the victim. One session of cardiopulmonary resuscitation includes 30 clicks on chest and 2 breaths from mouth to mouth. The procedure is carried out until signs of breathing and cardiac activity appear.

Identification of an allergic reaction is not an easy, but necessary process for providing competent first aid to the patient and drawing up an effective plan for further treatment. In clinical situations, the same reaction in different patients may have its own characteristics, despite the same mechanism of occurrence.

Therefore, it is quite difficult to establish an exact framework for the classification of allergies, as a result, many diseases are intermediate between the above categories.

It should be noted that the time of manifestation of an allergic reaction is not an absolute criterion for determining a specific type of disease, because. depends on a number of factors (Arthus phenomenon): the amount of the allergen, the duration of its exposure.

Types of allergic reactions

Depending on the time of occurrence of allergic reactions after contact with the allergen, they differentiate:

• immediate type allergy (symptoms occur immediately after contact of the body with the allergen or within a short period of time);
• delayed type allergy clinical manifestations occur within 1-2 days).

To find out which category the reaction belongs to, it is worth paying attention to the nature of the process of disease development, pathogenetic features.

Diagnosis of the main mechanism of allergy is necessary condition for the preparation of competent and effective treatment.

Allergy of the immediate type

An immediate type allergy (anaphylactic) occurs due to the reaction of antibodies of groups E (IgE) and G (IgG) with an antigen. The resulting complex is deposited on the mast cell membrane. This stimulates the body to increase the synthesis of free histamine. As a result of a violation of the regulatory process of the synthesis of immunoglobulins of group E, namely their excessive formation, there is an increased sensitivity of the body to the effects of stimuli (sensitization). The production of antibodies is directly dependent on the ratio of the amount of proteins that control the IgE response.

The causes of immediate hypersensitivity are often:

This type of allergy may occur due to the transfer healthy person the patient's blood serum.

Typical examples of an immediate immune response are:

• anaphylactic shock;
• bronchial asthma of allergic type;
• inflammation of the nasal mucosa;
• rhinoconjunctivitis;
• allergic rash;
• skin inflammation;

The first thing to do to relieve symptoms is to identify and eliminate the allergen. Mild allergic reactions such as hives and rhinitis are treated with antihistamines.

In case of severe diseases, glucocorticoids are used. If an allergic reaction develops rapidly in a severe form, it is necessary to call an ambulance.

The state of anaphylactic shock requires urgent medical care. It will be liquidated hormonal preparations such as adrenaline. During first aid, the patient should be laid on pillows to facilitate the breathing process.

The horizontal position also contributes to the normalization of blood circulation and pressure, while the upper body and head of the patient should not be raised. In case of respiratory arrest and loss of consciousness, resuscitation is necessary: indirect massage heart, mouth-to-mouth artificial respiration.

If necessary, in a clinical setting, the patient's trachea is intubated to supply oxygen.

delayed allergy

Delayed-type allergy (late hypersensitization) occurs over a longer period of time (days or more) after the body has come into contact with the antigen. Antibodies do not take part in the reaction; instead, the antigen is attacked by specific clones - sensitized lymphocytes formed as a result of previous intakes of the antigen.

Reciprocal inflammatory processes are caused by active substances secreted by lymphocytes. As a result, the phagocytic reaction is activated, the process of chemotaxis of macrophages and monocytes, inhibition of the movement of macrophages occurs, the accumulation of leukocytes in the inflammatory zone increases, the consequences lead to inflammation with the formation of granulomas.

This painful condition is often caused by:

• bacteria;
• fungal spores;
• opportunistic and pathogenic microorganisms (staphylococci, streptococci, fungi, pathogens of tuberculosis, toxoplasmosis, brucellosis);
• some substances containing simple chemical compounds (chromium salts);
• vaccinations;
• chronic inflammation.

Such an allergy is not transferred to a healthy person by the patient's blood serum. But leukocytes, cells of lymphoid organs and exudate can carry the disease.

Typical diseases are:

Delayed-type allergies are treated with drugs intended for the relief of systemic connective tissue diseases and immunosuppressants (immune suppressive drugs). The pharmacological group of drugs includes drugs prescribed for rheumatoid arthritis, systemic lupus erythematosus, nonspecific ulcerative prick. They suppress hyperimmune processes in the body caused by impaired tissue immunity.

Conclusions: main differences between types of allergic reactions

So, the main differences between immediate and delayed type allergies are as follows:

• pathogenesis of the disease, namely the transience of the development of the disease;
• the presence or absence of circulating antibodies in the blood;
• groups of allergens, their nature of origin, causes of occurrence;
• emerging diseases;
• disease treatment, pharmacological groups drugs indicated in the treatment different types allergies;
• the possibility of passive transmission of the disease.

According to modern concepts, all allergic reactions, all manifestations of allergies depending on the rate of occurrence and intensity of manifestation of clinical signs after a repeated meeting of the allergen with the body, they are divided into two groups:

* Allergic reactions of immediate type;

* Allergic reactions of the delayed type.

Allergic reactions of immediate type (immediate type hypersensitivity, anaphylactic type reaction, chimergic type reaction, B - dependent reactions). These reactions are characterized by the fact that antibodies in most cases circulate in body fluids, and they develop within a few minutes after repeated exposure to the allergen.

Allergic reactions of the immediate type proceed with the participation of antibodies formed in response to the antigenic load in circulating humoral media. Re-entry of the antigen leads to its rapid interaction with circulating antibodies, the formation of antigen-antibody complexes. According to the nature of the interaction of antibodies and the allergen, there are three types of immediate hypersensitivity reactions: first type - r e a g i n o v y, including anaphylactic reactions. The reinjected antigen meets with an antibody (Ig E) fixed on tissue basophils. As a result of degranulation, histamine, heparin, hyaluronic acid, kallecrein, and other biologically active compounds are released and enter the bloodstream. Complement does not take part in reactions of this type. The general anaphylactic reaction is manifested by anaphylactic shock, local - by bronchial asthma, hay fever, urticaria, Quincke's edema.

Second type - cytotoxic, characterized by the fact that the antigen is sorbed on the surface of the cell or represents some of its structure, and the antibody circulates in the blood. The resulting antigen-antibody complex in the presence of complement has a direct cytotoxic effect. In addition, activated killer immunocytes and phagocytes are involved in cytolysis. Cytolysis occurs with the introduction of large doses of antireticular cytotoxic serum. Cytotoxic reactions can be obtained in relation to any tissues of the recipient animal if it is injected with the blood serum of a donor previously immunized against them.

The third type is reactions of the Artyus phenomenon type. It was described by the author in 1903 in rabbits previously sensitized with horse serum after subcutaneous injection of the same antigen. Acute necrotizing inflammation of the skin develops at the injection site. The main pathogenetic mechanism is the formation of an antigen + antibody complex (Ig G) with the complement of the system. The formed complex must be large, otherwise it does not precipitate. At the same time, platelet serotonin is of great importance, which increases the permeability of the vascular wall, promotes the microprecipitation of immune complexes, their deposition in the walls of blood vessels and other structures. At the same time, there is always a small amount (Ig E) in the blood, fixed on basophils and mast cells. Immune complexes attract neutrophils, phagocytize them, they secrete lysosomal enzymes, which, in turn, determine the chemotaxis of macrophages. Under the influence of hydrolytic enzymes released by phagocytic cells (pathochemical stage), damage (pathophysiological stage) of the vascular wall, loosening of the endothelium, thrombosis, hemorrhages, and sharp disturbances of microcirculation with necrotic foci begin. Inflammation develops.

In addition to the Arthus phenomenon, serum sickness can serve as a manifestation of allergic reactions of this type.

Serum sickness- a symptom complex that occurs after parenteral administration of sera into the body of animals and humans for prophylactic or therapeutic purposes (anti-rabies, anti-tetanus, anti-plague, etc.); immunoglobulins; transfused blood, plasma; hormones (ACTH, insulin, estrogen, etc.) some antibiotics, sulfonamides; with the bites of insects that release toxic compounds. The basis for the formation of serum sickness are immune complexes that arise in response to the primary, single entry of the antigen into the body.

The properties of the antigen and the characteristics of the reactivity of the organism affect the severity of the manifestation of serum sickness. When a foreign antigen enters the animal, three types of response are observed: 1) antibodies are not formed at all and the disease does not develop; 2) there is a pronounced formation of antibodies and immune complexes. Clinical signs appear quickly, as the antibody titer increases, they disappear; 3) weak antibody genesis, insufficient elimination of the antigen. Favorable conditions are created for the long-term persistence of immune complexes and their cytotoxic effect.

Symptoms are characterized by pronounced polymorphism. The prodromal period is characterized by hyperemia, increased skin sensitivity, enlarged lymph nodes, acute pulmonary emphysema, damage and swelling of the joints, swelling of the mucous membranes, albuminuria, leukopenia, thrombocytopenia, increased ESR, hypoglycemia. In more severe cases, acute glomerulonephritis, myocardial dysfunction, arrhythmia, vomiting, and diarrhea are observed. In most cases, after 1-3 weeks, the clinical signs disappear and recovery occurs.

Bronchial asthma - It is characterized by a sudden attack of suffocation with a sharp difficulty in the expiratory phase as a result of a diffuse patency disorder in the system of small bronchi. Manifested by bronchospasm, swelling of the mucous membrane of the bronchi, hypersecretion of the mucous glands. In the atopic form, the attack begins with a cough, then a picture of expiratory suffocation develops, a large number of dry whistling rales are heard in the lungs.

Pollinosis (hay fever, allergic rhinitis) - a recurrent disease associated with the inhalation and conjunctiva of plant pollen from the air during their flowering period. It is characterized by hereditary predisposition, seasonality (usually spring-summer, due to the flowering period of plants). It is manifested by rhinitis, conjunctivitis, irritation and itching of the eyelids, sometimes general weakness, fever. An increased amount of histamine, reagins (Ig E), eosinophilic granulocytes, globulin fraction of blood serum, an increase in transaminase activity are detected in the blood. Attacks of the disease disappear after contact with plant allergens is stopped after a few hours, sometimes after a few days. The rhino-conjunctival form of pollinosis can end with a visceral syndrome, in which a number of internal organs are affected (pneumonia, pleurisy, myocarditis, etc.).

Urticaria and angioedema- occur when exposed to plant, pollen, chemical, epidermal, serum, drug allergens, house dust, insect bites, etc. This disease usually begins suddenly, with the manifestation of very often unbearable itching. At the site of scratching, hyperemia instantly occurs, then there is a rash on the skin of itchy blisters, which are swelling of a limited area, mainly the papillary layer of the skin. There is an increase in body temperature, swelling of the joints. The illness lasts from several hours to several days.

One type of urticaria is Quincke's edema (giant urticaria, angioedema). With Quincke's edema, skin itching usually does not occur, since the process is localized in the subcutaneous layer, not spreading to sensitive endings cutaneous nerves. Sometimes urticaria and Quincke's edema proceed very rapidly, preceding the development of anaphylactic shock. In most cases, the acute phenomena of urticaria and Quincke's edema are completely cured. Chronic forms are difficult to treat, characterized by an undulating course with alternating periods of exacerbation and remission. The generalized form of urticaria is very difficult, in which edema captures the mucous membrane of the mouth, soft palate, tongue, and the tongue hardly fits in the oral cavity, while swallowing is very difficult. In the blood, an increase in the content of eosinophilic granulocytes, globulins and fibrinogen, a decrease in the level of albumins are found.

General pathogenesis of immediate allergic reactions .

Allergic reactions of immediate type, different in external manifestations, have common mechanisms of development. In the genesis of hypersensitivity, three stages are distinguished: immunological, biochemical (pathochemical) and pathophysiological. Immunological stage begins with the first contact of the allergen with the body. The hit of the antigen stimulates macrophages, they begin to release interleukins that activate T-lymphocytes. The latter, in turn, trigger the processes of synthesis and secretion in B-lymphocytes, which turn into plasma cells. Plasma cells during the development of an allergic reaction of the first type produce mainly Ig E, the second type - Ig G 1,2,3, Ig M, the third type - mainly Ig G, Ig M.

Immunoglobulins are fixed by cells on the surface of which there are corresponding receptors - on circulating basophils, mast cells of the connective tissue, platelets, smooth muscle cells, skin epithelium, etc. A period of sensitization sets in, sensitivity to repeated exposure to the same allergen increases. The maximum severity of sensitization occurs after 15-21 days, although the reaction may occur much earlier. In the case of reinjection of the antigen to a sensitized animal, the interaction of the allergen with antibodies will occur on the surface of basophils, platelets, mast and other cells. When an allergen binds to more than two adjacent immunoglobulin molecules, the membrane structure is disrupted, the cell is activated, and previously synthesized or newly formed allergy mediators begin to be released. Moreover, only about 30% of the biologically active substances contained there are released from the cells, since they are ejected only through the deformed section of the target cell membrane.

AT pathochemical stage changes occurring on the cell membrane in the immunological phase due to the formation of immune complexes trigger a cascade of reactions, the initial stage of which is, apparently, the activation of cellular esterases. As a result, a number of allergy mediators are released and re-synthesized. Mediators have vasoactive and contractile activity, chemotoxic properties, the ability to damage tissues and stimulate repair processes. The role of individual mediators in the overall reaction of the body to repeated exposure to the allergen is as follows.

Histamine - one of the most important mediators of allergy. Its release from mast cells and basophils is carried out by secretion, which is an energy-dependent process. The energy source is ATP, which breaks down under the influence of activated adenylate cyclase. Histamine dilates capillaries, increases vascular permeability by dilating terminal arterioles and constricting postcapillary venules. It inhibits the cytotoxic and helper activity of T-lymphocytes, their proliferation, differentiation of B-cells and the synthesis of antibodies by plasma cells; activates T-suppressors, has a chemokinetic and chemotactic effect on neutrophils and eosinophils, inhibits the secretion of lysosomal enzymes by neutrophils.

Serotonin - mediates smooth muscle contraction, increased permeability and vasospasm of the heart, brain, kidneys, and lungs. Released in animals from mast cells. Unlike histamine, it does not have an anti-inflammatory effect. Activates the suppressor population of T-lymphocytes of the thymus and spleen. Under its influence, T-suppressors of the spleen migrate to Bone marrow and lymph nodes. Along with the immunosuppressive effect, serotonin can have an immunostimulating effect through the thymus. Enhances the sensitivity of mononuclear cells to various chemotaxis factors.

Bradykinin - the most active component of the kinin system. It changes the tone and permeability of blood vessels; lowers blood pressure, stimulates the secretion of mediators by leukocytes; to some extent affects the mobility of leukocytes; causes smooth muscle contraction. In asthmatic patients, bradykinin leads to bronchospasm. Many of the effects of bradykinin are due to a secondary increase in prostaglandin secretion.

Heparin - proteoglycan, which forms complexes with antithrombin, which prevent the coagulating effect of thrombin (blood clotting). It is released in allergic reactions from mast cells, where it is found in large quantities. In addition to anticoagulation, it has other functions: it participates in the reaction of cell proliferation, stimulates the migration of endothelial cells into the capillaries, inhibits the action of complement, activates pino- and phagocytosis.

Complement fragments - have anaphylactic (histamine-releasing) activity against mast cells, basophils, other leukocytes, increase the tone of smooth muscles. Under their influence, vascular permeability increases.

Slow-reacting substance of anaphylaxis (MRSA) - unlike histamine, causes a slow contraction of the smooth muscles of the trachea and ileum of a guinea pig, human and monkey bronchioles, increases the permeability of skin vessels, and has a more pronounced bronchospastic effect than histamine. The action of MRSA is not removed by antihistamines. It is secreted by basophils, peritoneal alveolar and blood monocytes, mast cells, various sensitized lung structures.

Protoglandins - prostaglandins E, F, D are synthesized in body tissues. Exogenous prostaglandins have the ability to stimulate or inhibit the inflammatory process, cause fever, dilate blood vessels, increase their permeability, and cause erythema. Prostaglandins F cause severe bronchospasm. Prostaglandins E have the opposite effect, having a high bronchodilating activity.

pathophysiological stage. It is a clinical manifestation of allergic reactions. Biologically active substances secreted by target cells have a synergistic effect on the structure and function of organs and tissues of the animal organism. The resulting vasomotor reactions are accompanied by blood flow disorders in the microcirculatory bed, and are reflected in the systemic circulation. Expansion of capillaries and an increase in the permeability of the histohematic barrier lead to the release of fluid beyond the walls of blood vessels, the development of serous inflammation. The defeat of the mucous membranes is accompanied by edema, hypersecretion of mucus. Many mediators of allergy stimulate the contractile function of the myofibrils of the walls of the bronchi, intestines, and other hollow organs. The results of spastic contractions of muscle elements can manifest themselves in asphyxia, disorders of the motor function of the gastrointestinal tract, such as vomiting, diarrhea, sharp pain from excessive contractions of the stomach and intestines.

The nervous component of the genesis of an immediate type of allergy is due to the influence of kinins (bradykinin), histamine, serotonin on neurons and their sensitive formations. Disorders of nervous activity with allergies can be manifested by fainting, a feeling of pain, burning, unbearable itching. Immediate-type hypersensitivity reactions end with either recovery or death, which may be caused by asphyxia or acute hypotension.

Delayed allergic reactions (hypersensitivity of the delayed type, hypersensitivity of the delayed type, T - dependent reactions). This form of allergy is characterized by the fact that antibodies are fixed on the membrane of lymphocytes and are receptors for the latter. Clinically detected 24-48 hours after the contact of the sensitized organism with the allergen. This type of reaction proceeds with the predominant participation of sensitized lymphocytes, therefore it is considered as a pathology. cellular immunity. The slowdown in the reaction to the antigen is explained by the need for a longer time for the accumulation of lymphocytic cells (T- and B - lymphocytes of different populations, macrophages, basophils, mast cells) in the area of ​​​​action of a foreign substance compared with the humoral reaction antigen + antibody with immediate type hypersensitivity. Delayed-type reactions develop with infectious diseases, vaccinations, contact allergies, autoimmune diseases, with the introduction of various antigenic substances into animals, and the application of haptens. They are widely used in veterinary medicine for allergic diagnosis of latent forms of chronic infectious diseases such as tuberculosis, glanders, and some helminthic infestations (echinococcosis). Delayed-type reactions are tuberculin and maleic allergic reactions, rejection of transplanted tissue, autoallergic reactions, bacterial allergies.

General pathogenesis of delayed-type allergic reactions

Delayed hypersensitivity occurs in three stages:

AT pathochemical stage stimulated T-lymphocytes synthesize a large number of lymphokines - mediators of HRT. They, in turn, involve other types of cells, such as monocytes / macrophages, neutrophils, in response to a foreign antigen. The most important in the development of the pathochemical stage are the following mediators:

the migration-inhibiting factor is responsible for the presence of monocytes/macrophages in the inflammatory infiltrate; it is assigned the most important role in the formation of the phagocytic response;

factors affecting macrophage chemotaxis, their adhesion, resistance;

mediators that affect the activity of lymphocytes, such as a transfer factor that promotes the maturation of T-cells in the body of the recipient after the introduction of sensitized cells; a factor that causes blast transformation and proliferation; a suppression factor that inhibits the immune response to an antigen, etc.;

a chemotaxis factor for granulocytes that stimulates their emigration, and an inhibitory factor that acts in the opposite way;

interferon, which protects the cell from the introduction of viruses;

skin-reactive factor, under the influence of which the permeability of the skin vessels increases, swelling, redness, tissue thickening at the site of antigen reinjection appear.

The influence of allergy mediators is limited by opposing systems that protect target cells.

AT pathophysiological stage biologically active substances released by damaged or stimulated cells determine the further development of delayed-type allergic reactions.

Local tissue changes in delayed-type reactions can be detected as early as 2-3 hours after exposure to a resolving dose of antigen. They are manifested by the initial development of a granulocytic reaction to irritation, then lymphocytes, monocytes and macrophages migrate here, accumulating around the vessels. Along with migration, cell proliferation takes place in the focus of an allergic reaction. However, the most pronounced changes are observed after 24-48 hours. These changes are characterized by hyperergic inflammation with pronounced signs.

Delayed allergic reactions are induced mainly by thymus-dependent antigens - purified and unpurified proteins, microbial cell components and exotoxins, virus antigens, low molecular weight protein-conjugated haptens. The reaction to the antigen in this type of allergy can be formed in any organ, tissue. It is not associated with the participation of the complement system. The main role in pathogenesis belongs to T-lymphocytes. The genetic control of the reaction is carried out either at the level of individual subpopulations of T- and B-lymphocytes, or at the level of intercellular relationships.

malleic allergic reaction used to detect glanders in horses. The application of purified mallein obtained from pathogens to the mucous membrane of the eye of infected animals after 24 hours is accompanied by the development of acute hyperergic conjunctivitis. At the same time, an abundant outflow of grayish-purulent exudate from the corner of the eye, arterial hyperemia, and swelling of the eyelids are observed.

transplanted tissue rejection as a result of transplantation of foreign tissue, the recipient's lymphocytes become sensitized (become carriers of the transfer factor or cellular antibodies). These immune lymphocytes then migrate to the transplant, where they are destroyed and release the antibody, which causes the destruction of the transplanted tissue. The transplanted tissue or organ is rejected. Transplant rejection is the result of a delayed-type allergic reaction.

Autoallergic reactions - reactions resulting from damage to cells and tissues by autoallergens, i.e. allergens that originate in the body itself.

Bacterial allergy - appears with preventive vaccinations and with certain infectious diseases (with tuberculosis, brucellosis, coccal, viral and fungal infections). If the allergen is administered intradermally to a sensitized animal, or applied to scarified skin, then the response begins no earlier than 6 hours later. At the site of contact with the allergen, hyperemia, induration and sometimes skin necrosis occur. With the injection of small doses of the allergen, necrosis is absent. In clinical practice, delayed skin reactions Pirquet, Mantoux are used to determine the degree of sensitization of the body in a particular infection.

Second classification. Depending on the type of allergen All allergies are divided into:

Serum

infectious

1. Vegetable

   Animal origin

   drug allergy

   Idiosyncrasy

   household allergies

   Autoallergy

Serum allergy. This is such an allergy that occurs after the introduction of any therapeutic serum. An important condition for the development of this allergy is the presence of an allergic constitution. Perhaps this is due to the peculiarity of the vegetative nervous system, blood histaminase activity and other indicators characterizing the body's setting for an allergic reaction.

This type of allergy is especially important in veterinary practice. Anti-erysipelas serum, with inept treatment causes the phenomenon of allergy, anti-tetanus serum can be an allergen, with repeated administration, anti-diphtheria serum can be an allergen.

The mechanism of development of serum sickness is that a foreign protein introduced into the body causes the formation of antibodies such as precipitins. Antibodies are partially fixed on the cells, some of them circulate in the blood. After about a week, the antibody titer reaches a level sufficient to react with a specific allergen for them - a foreign serum that is still preserved in the body. As a result of the combination of the allergen with the antibody, an immune complex arises, which settles on the endothelium of the capillaries of the skin, kidneys and other organs. This causes damage to the endothelium of the capillaries, an increase in permeability. Allergic edema, urticaria, inflammation of the lymph nodes, glomeruli of the kidneys and other disorders characteristic of this disease develop.

infectious allergy – such an allergy, when the allergen is any pathogen. This property may have a tubercle bacillus, pathogens of glanders, brucellosis, helminths.

Infectious allergy is used for diagnostic purposes. This means that microorganisms increase the body's sensitivity to preparations prepared from these microorganisms, extracts, extracts.

food allergy – various clinical manifestations of allergy associated with food intake. The etiological factor is food proteins, polysaccharides, low molecular weight substances acting as haptens (food allergens). The most common food allergies are to milk, eggs, fish, meat and products from these products (cheeses, butter, creams), strawberries, strawberries, honey, nuts, citrus fruits. Allergenic properties are possessed by additives and impurities contained in food products, preservatives (benzoic and acetylsalicylic acids), food colorings, etc.

There are early and late reactions of food allergies. Early ones develop within one hour from the moment of ingestion, severe anaphylactic shock is possible, up to death, acute gastroenteritis, hemorrhagic diarrhea, vomiting, collapse, bronchospasm, swelling of the tongue and larynx. Late manifestations of allergy are associated with skin lesions, dermatitis, urticaria, angioedema. Symptoms of food allergies are observed in different parts of the gastrointestinal tract. Possible development of allergic stomatitis, gingivitis, damage to the esophagus with symptoms of edema, hyperemia, rashes on the mucous membrane, feeling of difficulty swallowing, burning and soreness along the esophagus. The stomach is often affected. Such a lesion in the clinic is similar to acute gastritis: nausea, vomiting, pain in the epigastric region, tension abdominal wall, eosinophilia of gastric contents. With gastroscopy, swelling of the gastric mucosa is noted, hemorrhagic rashes are possible. With intestinal damage, there are cramping or persistent pain, bloating, tension in the abdominal wall, tachycardia, and a drop in blood pressure.

plant allergy – such an allergy, when the allergen is the pollen of a plant. Pollen of bluegrass meadow, cocksfoot, wormwood, timothy grass, meadow fescue, ragweed and other herbs. The pollen of various plants differs from each other in antigenic composition, but there are also common antigens. This causes the development of polyvalent sensitization caused by the pollen of many grasses, as well as the appearance of cross-reactions to various allergens in patients with hay fever.

The allergenic properties of pollen depend on the conditions in which it resides. Fresh pollen, i.e. when it is released into the air from the dust particles of the stamens of grasses and trees, it is very active. Getting into a humid environment, for example, on mucous membranes, the pollen grain swells, its shell bursts, and the internal contents - plasma, which has allergenic properties, is absorbed into the blood and lymph, sensitizing the body. It has been established that grass pollen has more pronounced allergenic properties than tree pollen. In addition to pollen, other parts of plants may have allergenic properties. The most studied of them are fruits (cotton).

Repeated contact with plant pollen can cause suffocation, bronchial asthma, inflammation of the upper respiratory tract, etc.

Allergy of animal origin- cells of various tissues, components of various structures of a living organism have pronounced allergenic properties. The most significant are epidermal allergens, Hymenoptera poisons and mites. Epidermal allergens consist of integumentary tissues: dandruff, epidermis and hair of various animals and humans, particles of claws, beaks, nails, feathers, animal hooves, scales of fish and snakes. Frequent allergic reactions in the form of anaphylactic shock from insect bites. The presence of cross-allergic reactions caused by insect bites has been shown within the class or species. Insect venom is a product of special glands. It consists of substances with pronounced biological activity: biogenic amines (histamine, dopamine, acetylcholine, norepinephrine), proteins and peptides. Allergens of ticks (bed, barn, dermatophagous, etc.) are often the cause of bronchial asthma. When they enter with the inhaled air, the sensitivity of the body is perverted.

drug allergy - when the allergen is any medicinal substance. Allergic reactions caused by drugs presently present the most serious complications in drug therapy. The most common allergens are antibiotics, especially administered orally (penicillin, streptomycin, etc.). Most drugs are not full antigens, but have the properties of haptens. In the body, they form complexes with blood serum proteins (albumin, globulin) or tissues (procollagen, histone, etc.). This indicates the ability of almost every drug or chemical to cause allergic reactions. In some cases, haptens are not antibiotics or chemotherapy drugs, but the products of their metabolism. Thus, sulfanilamide preparations do not have allergenic properties, but acquire them after oxidation in the body. A characteristic feature of medicinal allergens is their pronounced ability to cause paraspecific or cross-reactions, which causes polyvalence. drug allergy. Manifestations of drug allergies range from mild reactions in the form of skin rash and fever, to the development of anaphylactic shock.

Idiosyncrasy - (from Greek . idios - independent, syncrasis - mixing) is an innate hypersensitivity to food or drugs. When taking certain foods (strawberries, milk, chicken protein, etc.) or drugs (iodine, iodoform, bromine, quinine), certain individuals experience disorders. The pathogenesis of idiosyncrasy has not yet been established. Some researchers point out that in idiosyncrasy, unlike anaphylaxis, it is not possible to detect specific antibodies in the blood. It is assumed that food idiosyncrasy is associated with the presence of congenital or acquired increased permeability of the intestinal wall. As a result, protein and other allergens can be absorbed into the blood in an unsplit form and thereby sensitize the body to them. When the body encounters these allergens, an attack of idiosyncrasy occurs. In some people, characteristic allergic phenomena occur mainly from the skin and vascular system: hyperemia of mucous membranes, edema, urticaria, fever, vomiting.

household allergies - in this case, the allergen can be mold, sometimes fish food - dried daphnia, plankton (lower crustaceans), house dust, household dust, mites. Household dust is the dust of residential premises, the composition of which varies in terms of the content of various fungi, bacteria and particles of organic and inorganic origin. Library dust in large quantities contains remnants of paper, cardboard, etc. According to most modern data, the allergen from house dust is a mucoprotein and a glycoprotein. Household allergens can sensitize the body.

Autoallergy- occurs when allergens are formed from their own tissues. With the normal function of the immune system, the body removes, neutralizes its own, degenerate cells, and if the body's immune system cannot cope, then the degenerate cells and tissues become allergens, i.e. autoallergens. In response to the action of autoallergens, autoantibodies (reagins) are formed. Autoantibodies combine with autoallergens (self-antigens) and form a complex that damages healthy tissue cells. The complex (antigen + antibody) is able to settle on the surface of muscles, other tissues (brain tissue), on the surface of the joints and cause allergic diseases.

According to the mechanism of autoallergy, diseases such as rheumatism, rheumatic heart disease, encephalitis, collagenoses occur (non-cellular parts of the connective tissue are damaged), kidneys are affected.

The third classification of allergies.

Depending on the sensitizing agent There are two types of allergies:

* Specific

* Non-specific

Allergy is called specific if the sensitivity of the organism is perverted only to the allergen with which the organism is sensitized, i.e. there is strict specificity here.

A representative of a specific allergy is anaphylaxis. Anaphylaxis consists of two words (ana - without, phylaxis - protection) and literally translated - defenselessness.

Anaphylaxis- this is an increased and qualitatively perverted response of the body to the allergen to which the body is sensitized.

The first introduction of an allergen into the body is called sensitizing administration, or otherwise sensitizing. The value of the sensitizing dose can be very small, sometimes it is possible to sensitize with such a dose as 0.0001 g of the allergen. The allergen must enter the body parenterally, i.e., bypassing the gastrointestinal tract.

The state of increased sensitivity of the body or the state of sensitization occurs after 8-21 days (this is the time required for the production of class E antibodies), depending on the type of animal or individual characteristics.

A sensitized organism looks no different from an unsensitized organism.

Re-introduction of an antigen is called the introduction of a resolving dose or reinjection.

The size of the resolving dose is 5-10 times higher than the sensitizing dose, and the resolving dose should also be administered parenterally.

The clinical picture that occurs after the introduction of a resolving dose (according to Bezredko) is called anaphylactic shock.

Anaphylactic shock is a severe clinical manifestation of allergy. Anaphylactic shock can develop at lightning speed, within a few minutes after the introduction of the allergen, less often after a few hours. Harbingers of shock can be a feeling of heat, redness of the skin, itching, fear, nausea. The development of shock is characterized by a rapidly increasing collapse (pallor, cyanosis, tachycardia, thready pulse, cold sweat, a sharp decrease in blood pressure), suffocation, weakness, loss of consciousness, swelling of the mucous membranes, and convulsions. In severe cases, there is acute heart failure, pulmonary edema, acute kidney failure, allergic lesions of the intestines are possible, up to obstruction.

In severe cases, dystrophic and necrotic changes in the brain and internal organs, interstitial pneumonia, and glomerulonephritis may develop. At the height of shock in the blood, erythremia, leukocytosis, eosinophilia, an increase in ESR are noted; in the urine - proteinuria, hematuria, leukocyturia.

According to the rate of occurrence, anaphylactic shock can be (acute, subacute, chronic). acute form- Changes occur after a few minutes; subacute occurs after a few hours; chronic - changes occur after 2-3 days.

Different animal species do not show the same sensitivity to anaphylactic shock. The most sensitive to anaphylaxis are guinea pigs, and further on the degree of sensitivity, the animals are arranged in the following order - rabbits, sheep, goats, cattle, horses, dogs, pigs, birds, monkeys.

So, guinea pigs have anxiety, itching, scratching, sneezing, the pig rubs its muzzle with its paws, trembles, involuntary defecation is observed, takes a lateral position, breathing becomes difficult, intermittent, respiratory movements slow down, convulsions appear and may be fatal. This clinical picture is combined with a drop in blood pressure, a decrease in body temperature, acidosis, and an increase in the permeability of blood vessels. An autopsy of a guinea pig that died from anaphylactic shock reveals foci of emphysema and atelectasis in the lungs, multiple hemorrhages on the mucous membranes, and unclotting blood.

Rabbits - 1-2 minutes after the introduction of a resolving dose of serum, the animal begins to worry, shakes its head, lies on its stomach, shortness of breath appears. Then there is a relaxation of the sphincters and urine and feces are involuntarily separated, the rabbit falls, bends its head back, convulsions appear, then breathing stops, death occurs.

In sheep, anaphylactic shock is very acute. After the introduction of a permissive dose of serum, shortness of breath, increased salivation, lacrimation occur in a few minutes, pupils dilate. Swelling of the scar is observed, blood pressure decreases, involuntary separation of urine and feces appear. Then there are paresis, paralysis, convulsions, and often the death of the animal occurs.

In goats, cattle, and horses, the symptoms of anaphylactic shock are somewhat similar to those in the rabbit. However, they most clearly show signs of paresis, paralysis, and there is also a decrease in blood pressure.

Dogs. Essential in the dynamics of anaphylactic shock are disorders of the portal circulation and blood stasis in the liver and intestinal vessels. Therefore, anaphylactic shock in dogs proceeds according to the type of acute vascular insufficiency, at first there is excitement, shortness of breath, vomiting occurs, blood pressure drops sharply, involuntary separation of urine and feces, mostly red (an admixture of erythrocytes), appears. Then the animal falls into a stuporous state, while there is a bloody discharge from the rectum. Anaphylactic shock in dogs is rarely fatal.

In cats and fur-bearing animals (Arctic foxes, foxes, minks) similar dynamics of shock is observed. However, Arctic foxes are more susceptible to anaphylaxis than dogs.

Monkey. Anaphylactic shock in monkeys is not always reproducible. In shock, monkeys experience difficulty in breathing, collapse. The number of platelets falls, blood clotting decreases.

In the occurrence of anaphylactic shock, the functional state of the nervous system matters. It is not possible to cause a picture of anaphylactic shock in anesthetized animals (narcotic blocking of the central nervous system turns off impulses going to the site of allergen introduction), during hibernation, in newborns, with sudden cooling, as well as in fish, amphibians and reptiles.

Antianaphylaxis- this is a state of the body that is observed after suffering anaphylactic shock (if the animal has not died). This condition is characterized by the fact that the body becomes insensitive to this antigen (allergen within 8-40 days). The state of anti-anaphylaxis occurs 10 or 20 minutes after anaphylactic shock.

The development of anaphylactic shock can be prevented by administering small doses of the antigen to the sensitized animal 1-2 hours before the injection of the required volume of the drug. Small amounts of antigen bind antibodies, and the resolving dose is not accompanied by the development of immunological and other stages of immediate hypersensitivity.

Nonspecific Allergy- this is such a phenomenon when the body is sensitized to one allergen, and the sensitivity reaction to another allergen is perverted.

There are two types of nonspecific allergies (paraallergy and heteroallergy).

Paraallergy - they call such an allergy when the body is sensitized by one antigen, and sensitivity increases to another antigen, i.e. one allergen increases the sensitivity of the body to another allergen.

Heteroallergy is such a phenomenon when the body is sensitized by a factor of non-antigenic origin, and the sensitivity increases, perverts to any factor of antigenic origin, or vice versa. Factors of non-antigenic origin can be cold, exhaustion, overheating.

Cold can increase the body's sensitivity to foreign proteins, antigens. That is why in a state of cold, serum should not be administered; the flu virus shows its effect very quickly if the body is supercooled.

Fourth classification -according to the nature of the manifestation allergies are distinguished:

General- this is such an allergy, when, with the introduction of a resolving dose, the general condition of the body is disturbed, the functions of various organs and systems are disrupted. To obtain a general allergy, a single one-time sensitization is sufficient.

local allergy - this is such an allergy when, with the introduction of a resolving dose, changes occur at the injection site of the allergen, and at this site can develop:

hyperergic inflammation

ulceration

skin fold thickening

swelling

To obtain a local allergy, multiple sensitization is required with an interval of 4-6 days. If the same antigen is injected several times into the same place of the body with an interval of 4-6 days, then after the first injections, the antigen dissolves completely, and after the sixth, seventh injection, swelling, redness occurs at the injection site, and sometimes inflammatory reaction with extensive edema, extensive hemorrhage, i.e. local morphological changes are observed.

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Types of allergic reactions (hypersensitivity reactions). Hypersensitivity of the immediate and delayed type. Stages of allergic reactions. Step by step mechanism of development of allergic reactions.

1. 4 types of allergic reactions (hypersensitivity reactions).

Currently, according to the mechanism of development, it is customary to distinguish 4 types of allergic reactions (hypersensitivity). All these types of allergic reactions, as a rule, rarely occur in their pure form, more often they coexist in various combinations or move from one type of reaction to another type.
At the same time, types I, II and III are caused by antibodies, are and belong to immediate type hypersensitivity reactions (ITH). Type IV reactions are caused by sensitized T-cells and belong to delayed-type hypersensitivity reactions (DTH).

Note!!! is a hypersensitivity reaction triggered by immunological mechanisms. Currently, all 4 types of reactions are considered hypersensitivity reactions. However, true allergy is understood only as pathological immune reactions, which proceed according to the mechanism of atopy, i.e. according to type I, and reactions of types II, III and IV (cytotoxic, immunocomplex and cellular) types are classified as autoimmune pathology.

1. The first type (I) is atopic, anaphylactic or reaginic type - due to antibodies of the IgE class. When the allergen interacts with IgE fixed on the surface of mast cells, these cells are activated and the deposited and newly formed allergy mediators are released, followed by the development of an allergic reaction. Examples of such reactions are anaphylactic shock, angioedema, pollinosis, bronchial asthma, etc.
2. The second type (II) - cytotoxic. In this type, allergens become the body's own cells, the membrane of which has acquired the properties of autoallergens. This occurs mainly when they are damaged by drugs, bacterial enzymes or viruses, as a result of which the cells change and are perceived by the immune system as antigens. In any case, for this type of allergy to occur, antigenic structures must acquire the properties of self-antigens. The cytotoxic type is due to IgG- or IgM, which are directed against antigens located on the modified cells of the body's own tissues. The binding of At to Ag on the cell surface leads to the activation of complement, which causes damage and destruction of cells, subsequent phagocytosis and their removal. The process also involves leukocytes and cytotoxic T- lymphocytes. By binding to IgG, they are involved in the formation of antibody-dependent cellular cytotoxicity. It is by the cytotoxic type that the development of autoimmune hemolytic anemia, drug allergy, and autoimmune thyroiditis occurs.
3. The third type (III) - immunocomplex, in which body tissues are damaged by circulating immune complexes involving IgG- or IgM, which have a large molecular weight. That. in type III, as well as in type II, the reactions are due to IgG and IgM. But unlike type II, in a type III allergic reaction, antibodies interact with soluble antigens, and not with cells on the surface. The resulting immune complexes circulate in the body for a long time and are fixed in the capillaries of various tissues, where they activate the complement system, causing an influx of leukocytes, the release of histamine, serotonin, lysosomal enzymes that damage the vascular endothelium and tissues in which the immune complex is fixed. This type of reaction is the main one in serum sickness, drug and food allergies, in some autoallergic diseases (SLE, rheumatoid arthritis and etc).
4. The fourth (IV) type of reactions is delayed-type hypersensitivity or cell-mediated hypersensitivity. Delayed-type reactions develop in a sensitized organism 24-48 hours after contact with the allergen. In type IV reactions, the role of antibodies is performed by sensitized T- lymphocytes. Ag, contacting with Ag-specific receptors on T-cells, leads to an increase in the number of this population of lymphocytes and their activation with the release of mediators of cellular immunity - inflammatory cytokines. Cytokines cause the accumulation of macrophages and other lymphocytes, involve them in the process of destruction of AG, resulting in inflammation. Clinically, this is manifested by the development of hyperergic inflammation: a cellular infiltrate is formed, the cellular basis of which is mononuclear cells - lymphocytes and monocytes. The cellular type of reaction underlies the development of viral and bacterial infections ( contact dermatitis, tuberculosis, mycoses, syphilis, leprosy, brucellosis), some forms of infectious-allergic bronchial asthma, transplant rejection reactions and antitumor immunity.

2. Hypersensitivity of immediate and delayed type.

What is the fundamental difference between all these 4 types of allergic reactions?
And the difference lies in the predominant type of immunity - humoral or cellular - due to these reactions. Depending on this, there are:

3. Stages of allergic reactions.

In most patients, allergic manifestations are caused by IgE-class antibodies, therefore, we will also consider the mechanism of allergy development using the example of type I allergic reactions (atopy). There are three stages in their course:

• Immunological stage- includes changes in the immune system that occur at the first contact of the allergen with the body and the formation of appropriate antibodies, i.e. sensitization. If the allergen is removed from the body by the time At is formed, no allergic manifestations does not come. If the allergen enters repeatedly or continues to be in the body, an allergen-antibody complex is formed.
• pathochemical release of biologically active mediators of allergy.
• Pathophysiological- stage of clinical manifestations.

This division into stages is rather conditional. However, if you imagine allergy development step by step, it will look like this:

1. First contact with an allergen
2. Formation of IgE
3. Fixation of IgE on the surface of mast cells
4. Body sensitization
5. Repeated exposure to the same allergen and formation of immune complexes on the mast cell membrane
6. Release of mediators from mast cells
7. The action of mediators on organs and tissues
8. Allergic reaction.

Thus, the immunological stage includes points 1 - 5, the pathochemical stage - point 6, the pathophysiological stage - points 7 and 8.

4. Step-by-step mechanism for the development of allergic reactions.

1. First contact with an allergen.
2. Formation of 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 only combine with the allergen that caused their formation.
   But in the case of atopy, this is the formation of IgE to the incoming allergen, and in increased quantities in relation to other 5 classes of immunoglobulins, therefore it is also called Ig-E dependent allergy. IgE are produced locally, mainly in the submucosa of tissues in contact with the external environment: in respiratory tract, skin, gastrointestinal tract.
3. Fixation of IgE to the mast cell membrane.
   If all other classes of immunoglobulins circulate freely in the blood after their formation, then IgE has the property of immediately attaching to the mast cell membrane. Mast cells are immune cells connective tissue, which are found in all tissues in contact with the external environment: tissues of the respiratory tract, gastrointestinal tract, as well as connective tissues surrounding blood vessels. These cells contain such biologically active substances as histamine, serotonin, etc., and are called mediators of allergic reactions. They have a pronounced activity and have a number of effects on tissues and organs, causing allergic symptoms.
4. Body sensitization.
   For the development of an allergy, one condition is required - preliminary sensitization of the body, i.e. occurrence hypersensitivity to foreign substances - allergens. Hypersensitivity to this substance is formed at the first meeting with it.
   The time from the first contact with the allergen until the onset of hypersensitivity to it is called the sensitization period. It can range from a few days to several months or even years. This is the period during which IgE accumulates in the body, fixed to the membrane of basophils and mast cells.
   A sensitized organism is one that contains a stock of antibodies or T-lymphocytes (in the case of HRT) that are sensitized to that particular antigen.
   Sensitization is never accompanied by clinical manifestations of allergy, since only antibodies accumulate during this period. Immune complexes Ag + Ab have not yet formed. Damage to the tissue, causing an allergy, is capable not of single Abs, but only of immune complexes.
5. Repeated contact with the same allergen and the formation of immune complexes on the mast cell membrane.
   Allergic reactions occur only when the sensitized organism repeatedly encounters this allergen. Allergen binds to already prepared Abs on the surface of mast cells and immune complexes are formed: allergen + Abs.
6. Release of allergy mediators from mast cells.
   Immune complexes damage the membrane of mast cells, and from them, allergy mediators enter the intercellular environment. Tissues rich in mast cells (skin vessels, serous membranes, connective tissue, etc.) are damaged by released mediators.
   With prolonged exposure to allergens, the immune system uses extra cells to fend off the invading antigen. Another row is formed chemical substances– mediators, which causes further discomfort for allergy sufferers and increases the severity of symptoms. At the same time, the mechanisms of inactivation of allergy mediators are inhibited.
7. The action of mediators on organs and tissues.
   The action of mediators determines the clinical manifestations of allergy. Systemic effects develop - expansion of blood vessels and an increase in their permeability, mucous secretion, nerve stimulation, spasms of smooth muscles.
8. Clinical manifestations of an allergic reaction.
   Depending on the body, the type of allergens, the route of entry, the place where the allergic process is played out, the effects of one or another allergy mediator, symptoms can be systemic (classic anaphylaxis) or localized in individual body systems (asthma - in the respiratory tract, eczema - in the skin ).
   There are itching, runny nose, lacrimation, swelling, shortness of breath, pressure drop, etc. And the corresponding picture of allergic rhinitis, conjunctivitis, dermatitis, bronchial asthma or anaphylaxis develops.

In contrast to the immediate hypersensitivity described above, delayed-type allergy is caused by sensitized T cells and not by antibodies. And with it, those cells of the body on which the immune complex Ag + sensitized T-lymphocyte has been fixed are destroyed.

Abbreviations in the text.

• Antigens - Ag;
• Antibodies - At;
• Antibodies = same as immunoglobulins(At=Ig).
• Delayed type hypersensitivity - HRT
• Immediate type hypersensitivity - HNT
• Immunoglobulin A - IgA
• Immunoglobulin G - IgG
• Immunoglobulin M - IgM
• Immunoglobulin E - IgE.
• Immunoglobulins— Ig;
• Reaction of an antigen with an antibody - Ag + Ab