Autoimmune diseases. Mechanisms of autoimmune diseases Mechanisms of activation of autoimmune processes

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Autoimmune diseases. Mechanisms of development.Clinical forms. Autoantigens

Autoimmune diseases

Autoimmune diseases are a group of diseases in which the body's organs and tissues are destroyed by the body's own immune system.

The basis of autoallergic (autoimmune) diseases (ADs) are increased immune reactions to the molecular components of one’s own tissues and organs, which act as antigens.

Ra mechanismdevelopment of autoimmune diseases

The causes and mechanisms of development of AD are varied. Based on their origin, they distinguish between primary, genetically determined AD and secondary, resulting from viral infections, exposure to drugs and other factors. Autoallergic (autoimmune) reactions develop according to patterns similar to exogenous allergies and include immediate (immediate-type hypersensitivity - IFHT) and delayed (delayed-type hypersensitivity - IFH) reactions of all types.

Due to the commonality of the mechanisms of their development and the essence of the processes, autoimmune reactions are more correctly designated as autoallergic.

Anaphylactic , IgE-dependent reactions are not typical for AD.

Cytotoxic reactions are usually accompanied by autoantibodies against blood cell membranes, which are destroyed with the participation of complement. This type of reaction is observed in autoimmune anemia, neutropenia, systemic lupus erythematosus (lymphopenia).

Immunocomplex p These reactions lead to damage to the vascular network - vasculitis. They usually develop when many small immune complexes (with low affinity antibodies) are formed. These complexes are poorly eliminated from the bloodstream, which is facilitated by the deficiency of CR1 receptors of erythrocytes that bind the C3b component of complement in the immune complex, as well as a decrease in the activity of phagocytes, especially in the spleen. Immune complexes are deposited in the walls of blood vessels (capillaries). The organ localization (joints, kidneys, lungs) of their deposits usually depends on the type of antigen included in their composition. Small complexes penetrate the basement membrane and are deposited subepithelially (more kidney damage), and large complexes - under the basement membrane of the epithelium and subendothelial (better prognosis, less kidney damage).

Antireceptor reactions are caused by the binding of antibodies to functionally active cellular receptors. The pathology occurs due to an increase or decrease in the functions of the corresponding target cells: thyrotoxicosis, myasthenia gravis, insulin-dependent diabetes, pernicious anemia, idiopathic urticaria.

Delayed hypersensitivity (T-cell reactions) underlies many ADs. Moreover, its tuberculin variant predominates with infiltration of the affected tissue or organ with mononuclear cells. Often this variant, with a predominance of type 1 CD4 and CD8 lymphocytes in the infiltrates, is observed in the late phases of the autoallergic process, when the pancreatic islets in diabetes, thyroid follicles in thyroiditis and the structures of other organs are destroyed.

For raThe development of AZ requires a number of conditions

Genetic predisposition associated with genes of the HLA system and the corresponding phenotype, realized through the interaction of SI cells, target cells and agents tropic to them (viruses, substances, etc.);

The presence of unfavorable chemical, physical and biological factors that stimulate autoallergy;

Exposure to agents that are tropic to target cells (for example, viruses that have common epitopes with autologous organ-specific molecules - hormones, enzymes, cytokines, etc.); autoimmune autoallergic disease clinical

Genetically determined presence of sufficiently affinity variants of variable chains (and active centers) of receptors on T- and B-lymphocytes for organ-specific molecules, and therefore the potential ability of lymphocytes to form clones of autoreactive cells.

The functionality of the immune system is largely determined by hereditary factors, which is why many autoimmune diseases are passed on from generation to generation. The function of the immune system may be impaired under the influence of external factors such as infections, injuries, stress. At the moment, it is believed that unfavorable external factors, as such, are not capable of causing the development of an autoimmune disease, but only increase the risk of its development in individuals with a hereditary predisposition to this type of pathology.

Normally, in the body against the cells of all tissues there are small amounts of natural IgM autoantibodies, synthesized by CD5 + B1- lymphocytes, which do not cause pathological processes, but stimulate the regeneration of these tissues.

For autoallergic, increased reactions, it is necessary

· increase in their number

the appearance of IgG class antibodies,

· strengthening their specificity, avidity against certain structures.

For example, in thyrotoxicosis, these are antibodies against thyroglobulin receptors of thyrocytes, stimulating the synthesis of thyroid hormones. For autoimmune hemolytic anemia - antibodies against red blood cells, for neutropenia - against neutrophils, etc.

Cells of endocrine organs serve as an example of structures (“barrier organs”) that had no contact with cells of the immune system 30 in the embryonic period, when natural tolerance is formed. Therefore, antibodies to them and their molecules are easily formed in the event of damage by any agent - viruses, bacteria, or even physical, mechanical impact. To do this, it is enough for antigen molecules from the damaged endocrine organ to enter the blood or lymph and subsequent contact with immunocompetent cells.

The accumulation of highly specific autoreactive clones of T- and B-lymphocytes in connection with the stimulation of single, always persistent autospecific cells serves as the basis for the development of an autoallergic reaction. Such T-lymphocytes, carrying low-specific receptors, also exist normally. However, even if they penetrate and come into contact with the cells of endocrine organs, they undergo apoptosis (programmed cell death).

The fact is that the cells of the “behind-barrier organs,” which include endocrine ones, carry LCD95 on their surface (a ligand for the Fas receptor CD95), which, when interacting with the CD95 receptor on the T lymphocyte, causes its apoptosis. If cells of endocrine organs, for some reason (perhaps due to immunomodulation by a virus) lose LCD95 (this is observed in Hashimoto's thyroiditis), they can be destroyed by autoreactive T lymphocytes.

Features of triggering autoallergic diseases

Viruses, bacteria (their toxins), and environmentally harmful agents can trigger autoallergic diseases in several ways:

1) damaging cells and causing the release of “barrier” antigens into the lymph and blood, which directly stimulate an autoallergic reaction;

2) activating those T- and B-lymphocytes whose receptors cross-react with cells of tissues and organs carrying epitopes common to infectious agents (antigenic mimicry);

3) acting as superantigens and causing polyclonal activation of lymphocytes, i.e. binding to the V-chain of the T-cell receptor and activating up to 30% of T-lymphocytes, which release inflammatory cytokines (typical of bacterial toxins);

4) causing, in connection with an allergy to infectious antigens, activation of T- and B-lymphocytes with the formation of antibodies of varying specificity and a wide range of cytokines that trigger inflammation and/or leading to persistent immunomodulation (gamma interferon induced by the virus leads to the appearance on -cells of the pancreas HLA class II antigens);

5) inducing mutations and/or activation of cytokine genes involved in inflammation and cell damage;

6) inducing changes in T-lymphocyte homing due to suppression or stimulation of adhesion molecules and chemokine receptors;

7) inducing or inhibiting apoptosis of certain subpopulations of SI cells and/or target cells;

8) disrupting the regulation of the idiotype-anti-idiotypic network;

9) stimulating the formation of abzymes by B lymphocytes - antibodies with enzymatic activity that damage cell membranes.

Examples of autoantigenes, autoantibodies and their effects

Systemic lupus erythematosus. In SLE, the autoantigen is one's own DNA. Autoantibodies are antinuclear and anti-DNA. They cause cell lysis and the formation of immune complexes, complement activation, and cell damage.

Rheumatoid arthritis - IgM antibodies against autologous IgG (RF-rheumatoid factor), the formation of immune complexes that settle mainly in the joint cavities.

Pemphigus vulgaris IgG4 - antibodies to desmoglein-3 (cadherin) of the epidermis, epidermal detachment.

Goodpasture syndrome - antibodies to type II collagen of basement membranes, epithelium, kidneys and lungs, damage to these membranes.

Pernicious anemia - antibodies against intrinsic Castle factor block the binding of vitamin B12, inducing anemia.

Hyperthyroidism (thyrotoxicosis - Grevs-Bazedow disease) - antibodies to the receptor for thyroid-stimulating hormone stimulate the production of thyroid hormones - thyrotoxicosis syndrome (tachycardia, bulging eyes, etc.).

Myasthenia gravis - antibodies to the acetylcholine receptor, block the transmission of nerve impulses to the muscle - atrophy, muscle weakness.

Insulin-dependent diabetes type I - antibodies to pancreatic cells and their enzymes - cell damage.

Insulin-dependent diabetes type II - antibodies against insulin receptors - metabolic disorder.

Chronic idiopathic urticaria - antibodies to Fc type I (high-affinity receptor for IgE on basophils) - degranulation of basophils - rash.

Autoimmune hemolytic anemia - anti-erythrocyte antibodies - erythrocyte lysis.

Clinical forms

The clinical progression of the disease and symptoms of the disease can provide useful information for establishing the diagnosis of an autoimmune disease. The development of scleroderma is characterized by skin damage (foci of limited edema, which slowly undergo compaction and atrophy, the formation of wrinkles around the eyes, smoothing of the skin texture), damage to the esophagus with impaired swallowing, thinning of the terminal phalanges of the fingers, diffuse damage to the lungs, heart and kidneys. Lupus erythematosus is characterized by the appearance on the skin of the face (on the back of the nose and under the eyes) of a specific redness in the form of a butterfly, damage to the joints, the presence of anemia and thrombocytopenia. Rheumatism is characterized by the appearance of arthritis after a sore throat and the later formation of defects in the valvular apparatus of the heart.

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The immune system

The immune system is a system that protects the body from external invaders, and also ensures the functioning of the circulatory system and much more. Invading elements are recognized as foreign and this triggers a protective (immune) response.

The invading elements are called antigens. Viruses, bacteria, fungi, transplanted tissues and organs, pollen, chemicals - all these are antigens. The immune system is made up of specialized organs and cells located throughout the body. In terms of complexity, the immune system is slightly inferior to the nervous system.

The immune system, which destroys all foreign microorganisms, must be tolerant to the cells and tissues of its “host”. The ability to distinguish “self” from “foreign” is the main property of the immune system.

But sometimes, like any multicomponent structure with subtle regulatory mechanisms, it malfunctions - it mistakes its own molecules and cells for foreign ones and attacks them. Today, more than 80 autoimmune diseases are known; and in the world hundreds of millions of people are sick with them.

Tolerance to its own molecules is not inherent in the body initially. It is formed during fetal development and immediately after birth, when the immune system is in the process of maturation and “training”. If a foreign molecule or cell enters the body before birth, then it is perceived by the body as “self” for life.

At the same time, in the blood of every person, among billions of lymphocytes, “traitors” periodically appear that attack the body of their owner. Normally, such cells, called autoimmune or autoreactive, are quickly neutralized or destroyed.

Mechanism of development of autoimmune diseases

The mechanisms for the development of autoimmune reactions are the same as in the immune response to foreign agents, with the only difference being that the body begins to produce specific antibodies and/or T-lymphocytes that attack and destroy the body’s own tissues.

Why is this happening? To date, the causes of most autoimmune diseases remain unclear. Both individual organs and body systems may be “under attack.”

Causes of autoimmune diseases

The production of pathological antibodies or pathological killer cells may be associated with infection of the body with such an infectious agent, the antigenic determinants (epitopes) of the most important proteins of which resemble the antigenic determinants of normal tissues of the host body. It is by this mechanism that autoimmune glomerulonephritis develops after a streptococcal infection, or autoimmune reactive arthritis after gonorrhea.

An autoimmune reaction may also be associated with tissue destruction or necrosis caused by an infectious agent, or a change in their antigenic structure so that the pathologically altered tissue becomes immunogenic for the host. It is by this mechanism that autoimmune chronic active hepatitis develops after hepatitis B.

The third possible cause of an autoimmune reaction is a violation of the integrity of tissue (histo-hematological) barriers that normally separate some organs and tissues from the blood and, accordingly, from the immune aggression of the host lymphocytes.

Moreover, since normally the antigens of these tissues do not enter the blood at all, the thymus normally does not produce negative selection (destruction) of autoaggressive lymphocytes against these tissues. But this does not interfere with the normal functioning of the organ as long as the tissue barrier separating the organ from the blood is intact.

It is by this mechanism that chronic autoimmune prostatitis develops: normally the prostate is separated from the blood by the blood-prostatic barrier, prostate tissue antigens do not enter the blood, and the thymus does not destroy “anti-prostatic” lymphocytes. But with inflammation, injury or infection of the prostate, the integrity of the blood-prostatic barrier is disrupted and auto-aggression against prostate tissue can begin.

Autoimmune thyroiditis develops by a similar mechanism, since normally the thyroid colloid also does not enter the bloodstream (blood-thyroid barrier), only thyroglobulin with associated T3 and T4 is released into the blood.

There are known cases when, after suffering a traumatic amputation of an eye, a person quickly loses his second eye: immune cells perceive the tissues of a healthy eye as an antigen, since before this they lysed the remains of the tissues of the destroyed eye.

The fourth possible cause of the body’s autoimmune reaction is a hyperimmune state (pathologically enhanced immunity) or an immunological imbalance with a violation of the “selective” function of the thymus that suppresses autoimmunity or with a decrease in the activity of the T-suppressor subpopulation of cells and an increase in the activity of killer and helper subpopulations.

Symptoms of autoimmune diseases

Symptoms of autoimmune diseases can vary greatly depending on the type of disease. Several blood tests are usually required to confirm whether a person has an autoimmune disorder. Autoimmune diseases are treated with drugs that suppress the activity of the immune system.

Antigens can be contained in cells or on the surface of cells (eg bacteria, viruses or cancer cells). Some antigens, such as pollen or food molecules, exist on their own.

Even healthy tissue cells can have antigens. Normally, the immune system reacts only to antigens of foreign or dangerous substances, but as a result of certain disorders, it can begin to produce antibodies to normal tissue cells - autoantibodies.

An autoimmune reaction can lead to inflammation and tissue damage. Sometimes, however, autoantibodies are produced in such small quantities that autoimmune diseases do not develop.

Diagnosis of autoimmune diseases

Diagnosis of autoimmune diseases is based on determining the immune factor that causes damage to organs and tissues of the body. Such specific factors have been identified for most autoimmune diseases.

To determine these markers, various laboratory immunological research methods are used. The clinical progression of the disease and symptoms of the disease can provide useful information for establishing the diagnosis of an autoimmune disease.

Lupus erythematosus is characterized by the appearance on the skin of the face (on the back of the nose and under the eyes) of a specific redness in the form of a butterfly, damage to the joints, the presence of anemia and thrombocytopenia. Rheumatism is characterized by the appearance of arthritis after a sore throat and the later formation of defects in the valvular apparatus of the heart.

Treatment of autoimmune diseases

To treat autoimmune disorders, drugs that suppress the activity of the immune system are used. However, many of these medications interfere with the body's ability to fight disease. Immunosuppressants, such as azathioprine, chlorambucil, cyclophosphamide, cyclosporine, mofetil and methotrexate, often need to be taken for a long time.

During such therapy, the risk of developing many diseases, including cancer, increases. Corticosteroids not only suppress the immune system, but also reduce inflammation. The course of taking corticosteroids should be as short as possible - with long-term use they cause many side effects.

Etanercept, infliximab, and adalimubab block the activity of tumor necrosis factor, a substance that can cause inflammation in the body. These drugs are very effective in treating rheumatoid arthritis, but they can be harmful if used to treat certain other autoimmune diseases, such as multiple sclerosis.

Sometimes plasmapheresis is used to treat autoimmune diseases: abnormal antibodies are then removed from the blood, after which the blood is transfused back to the person. Some autoimmune diseases go away over a period of time as suddenly as they begin. However, in most cases they are chronic and often require lifelong treatment.

Descriptions of autoimmune diseases

Questions and answers on the topic "Autoimmune diseases"

Question:Hello. I was diagnosed with PSA and prescribed Methodject 10 times a week for 3 years. What risk to my body will I take while taking this medicine?

Answer: You can find this information in the instructions for use of the drug in the sections: “Side effects”, “Contraindications” and “Special instructions”.

Question:Hello. How should I manage my life after being diagnosed with an autoimmune disease?

Answer: Hello. Although most autoimmune diseases will not go away completely, you can take symptomatic treatment to control the disease and continue to enjoy life! Your life goals shouldn't change. It is very important to see a specialist for this type of disease, follow the treatment plan and lead a healthy lifestyle.

Question:Hello. Concerns about nasal congestion and malaise. The immune status refers to an autoimmune process in the body. Also about the chronic inflammatory process. In December, a diagnosis of tonsillitis was made, cryotherapy of the tonsils was performed, but the problem remained. Should I continue to be treated by an ENT specialist or look for an immunologist? Can this be cured at all?

Answer: Hello. In a situation where there is a chronic infection and changes in the immune status, you need to be treated by both an immunologist and an ENT specialist - everyone does their own thing, but in full agreement and understanding of the problem. In most cases, good results can be achieved.

Question:Hello, I'm 27 years old. I have been diagnosed with autoimmune thyroiditis for 7 years now. I was prescribed to take L-thyroxin 50 mcg tablets regularly. But I heard and read articles that this drug severely damages the liver and that in the West doctors prescribe it for a course of no more than 2 months. Please tell me, do I need to constantly take L-thyroxin or is it really better sometimes, in courses?

Answer: L-thyroxine is a completely safe drug, approved for use in children from infancy and pregnant women. I don’t know what articles and where you read about the negative effects of L-thyroxine, but we prescribe it for long-term use if necessary. The decision is made based on hormone levels.

Question:I am 55 years old. There is no hair anywhere for 3 years. The cause of alopecia universalis could not be determined. Perhaps the reason is an autoimmune process. What does this come from? How to check for an autoimmune disease? What is the connection with alopecia? What tests should I take, which specialist should I contact?

Answer: Trichologists deal with hair diseases. You should probably contact such a specialist. To identify the presence of an autoimmune disease, you need to pass (a minimum set of examinations) a general blood test, protein and protein fractions, do an immunogram (CD4, CD8, their ratio), based on the results of this examination, the doctor will decide whether to continue a more in-depth search for the autoimmune process. Modern science does not have an exact answer to the rest of your questions, there are only assumptions, let’s go back to the beginning, trichologists understand this problem better than anyone else.

AUTOIMMUNE DISEASES

KEY STUDY QUESTIONS

1. Immunopathological processes. Definition.

2. Pathological changes in the thymus gland that occur due to disorders of immunogenesis.

3. Accidental transformation of the thymus gland. Phases. Morphological changes.

4. Morphological changes in peripheral lymphoid tissue that occur due to disorders of immunogenesis.

5. Hypersensitivity reactions. Definition. Mechanisms of development. Morphological characteristics.

6. Autoimmunization. Definition. The concept of immunological tolerance. Etiology and pathogenesis of autoimmunization.

7. Autoimmune diseases. Groups of autoimmune diseases, diseases included in each group.

8. Immunodeficiency syndromes. Classification. Main primary immunodeficiency syndromes. Morphological features.

9. Secondary immunodeficiency syndromes. Reasons for development. Pathomorphology.

10. AIDS. Etiology. Pathogenesis. Stages of disease development. Morphological changes in the body.

SUPPORTING MATERIALS ON THE TOPIC

MICROPREPARATIONS: 1. Hashimoto's goiter (No. 23).

2. Accidental transformation

MATERIALS FOR CONTROL

PRACTICAL PART

Terminology

Accidental (from Latin accidentis - accident) - random.

Involution is reverse development.

Hypoplasia is underdevelopment of a tissue or organ.

Aplasia is a congenital absence of an organ.

Bursa-dependent (from Latin bursa - bag).

Thymus dependent (thymus - thymus gland).

T-helper cells (from help - help) are helpers.

Killer T cells (from killer) are killers.

Suppressor T cells (from suppression) are blockers.

Immunopathological are processes whose development is associated with dysfunction of immunocompetent (lymphoid) tissue. The morphology of immunopathological processes includes the structural expression of disorders of immunogenesis (antigenic stimulation or immune deficiency) and local immune reactions occurring in a sensitized organism - hypersensitivity reactions.

The morphology of immunogenesis disorders may affect the thymus and peripheral lymphoid tissue.

Changes in the thymus gland arising from disorders of immunogenesis are represented by the following processes:

1. aplasia;

2. hypoplasia;

3. dysplasia;

4. accidental involution;

5. atrophy;

6. thymomegaly;

7. hyperplasia with lymphoid follicles.

Aplasia, hypoplasia and dysplasia are congenital malformations of the thymus and are characterized primarily by a deficiency of the cellular component of immunity.

Thymic hormones are absent or produced in small quantities. The size of the gland is usually reduced (with aplasia there is no thymus), division into the cortex and medulla is impaired, and the number of lymphocytes is reduced.

Accidental involution characterized by a decrease in the lobes of the thymus gland, and, accordingly, the mass of the organ due to the loss of lymphocytes of the cortical zone with subsequent collapse of the organ.

Accidental transformation occurs under various stress influences, during fasting, X-ray irradiation, under the influence of drugs, in particular hormonal and cytostatic drugs. However, most often it is observed in infectious diseases, hemoblastosis and malignant tumors in children.

There are 5 main phases of changes in the thymus gland (Ivanovskaya T.E., 1978).

The 1st phase corresponds to the unchanged thymus gland of a healthy child.

The 2nd phase is characterized by a nested loss of lymphocytes from the cortex and their adhesion to macrophages, which creates the impression of a “starry sky”.

The 3rd phase is characterized by a further loss of lymphocytes from the cortex, which leads to an inversion of the layers - the medulla becomes richer in lymphocytes compared to the cortex. The reticuloepithelium is activated, and new formation of many thymic bodies is noted.

In the 4th phase, increasing collapse of the lobules occurs, the layers become indistinguishable, the thymic bodies are large, often forming cystic cavities.

In the 5th phase, the lobules look like narrow cords, the connective tissue layers are expanded, there are few lymphocytes and thymic bodies, many of them are calcified, which can be regarded as acquired atrophy.

MICROPREPARATION “Accidental transformation of the thymus” (hematoxylin-eosin staining). The division of the thymus gland into the cortical and medulla layers is indistinguishable due to the loss of leukocytes in the medulla. The collapse of the lobules is pronounced. The thymic corpuscles are fused and form large cystic dilated formations containing a pale colored protein secretion with scaly spherical inclusions and nuclear detritus. In some places, calcification of thymic bodies is observed. The connective tissue septa are dilated and swollen.

Atrophy thymus gland is a common cause of acquired immunodeficiency conditions. It is characterized by a decrease in the volume of parenchyma lobules, calcification of Hassall's bodies, proliferation of connective and adipose tissue in the perivascular spaces, followed by collapse of the lobules.

Timomegaly characterized by an increase in the mass and volume of the parenchyma while maintaining the normal structure. May be congenital or acquired. Microscopically, hyperplasia of lymphoid tissue is noted. The level of thymic hormones is reduced. The death of patients with thymomegaly often occurs from infectious or infectious-allergic diseases; sudden death syndrome may develop in children.

Hyperplasia with lymphoid follicles characterized by the appearance in the thymus tissue of lymphoid follicles that are not normally found.

Changes in peripheral lymphoid tissue upon antigenic stimulation, they are characterized by a macrophage reaction, lymphocyte hyperplasia followed by plasmacytic transformation.

With hereditary deficiency of peripheral lymphoid tissue in the spleen and lymph nodes, there is a decrease or disappearance of follicles, the absence of the cortical layer (B-dependent zone) of the lymph nodes, while maintaining the pericortical layer (T-dependent zone).

Hypersensitivity is a pathological overly strong immune reaction to a foreign agent, which leads to damage to body tissues.

Hypersensitivity reactions- these are local immune (allergic) reactions that occur in a sensitized body.

The following mechanisms are distinguished:

1. Immediate anaphylactic reaction (reaginic), associated with IgE. Features are the speed of development, the predominance of alterative and vascular-exudative changes, and the slow course of reparative processes.

2. Antibody-dependent cytotoxicity.

3. Reaction of immune complexes.

4. Delayed hypersensitivity reaction (associated with the effect of sensitized lymphocytes and macrophages on tissue, causing cytolysis).

5. Antibody-dependent functional changes (Graves disease, myasthenia gravis).

HYPERSENSITIVITY I (IMMEDIATE) TYPE

Development mechanism: the first arrival of an antigen (allergen) activates the immune system, which leads to the synthesis of antibodies - IgE (reagins), which have a specific reactivity against this antigen. They are then fixed on the surface membrane of tissue basophils and blood basophils due to the high affinity of IgE for Fc receptors. The synthesis of antibodies in sufficient quantities for the development of hypersensitivity takes one or more weeks. With subsequent administration of the same antigen, the antibody (IgE) interacts with the antigen on the surface of tissue or blood basophils, causing their degranulation. Vasoactive substances (histamine and various enzymes that are involved in the synthesis of bradykinin and leukotrienes) are released into the tissue from the cytoplasmic granules of tissue basophils, which cause vasodilation, increased vascular permeability and contraction of smooth muscles. Tissue basophils also secrete factors that are chemotactic for neutrophils and eosinophils; When studying preparations from tissues where a type I hypersensitivity reaction occurred, a large number of eosinophils are determined, and an increase in the number of eosinophils is observed in the blood of patients. Eosinophils activate both blood coagulation and the complement system and promote further degranulation of blood basophils and tissue basophils. However, eosinophils also secrete arylsulfatase B and histaminase, which degrade leukotrienes and histamine, respectively; thus they weaken the allergic response.

violations, occurring with type I hypersensitivity:
- local manifestations– atopy - is an innate predisposition to a pathological response against certain allergens. Atopic reactions are widespread and can occur in many organs.
When an allergen enters the skin, there is immediate redness, swelling (sometimes with blistering [urticaria]) and itching; in some cases, acute dermatitis or eczema develops. The antigen can come into contact with the skin directly, through injection (including insect bites) or orally into the body (with food and drug allergies). When an allergen is inhaled (for example, plant pollen, animal hair), vasodilation and hypersecretion of mucus occurs in the nasal mucosa (allergic rhinitis). Inhalation of allergens (pollen, dust) leads to contraction of bronchial smooth muscles and hypersecretion of mucus, which leads to acute airway obstruction and suffocation (allergic bronchial asthma). Oral ingestion of an allergen (for example, nuts, shellfish, crabs) causes contraction of the intestinal muscles and secretion of fluid, which manifests itself in the form of cramping abdominal pain and diarrhea (allergic gastroenteritis).
- systemic manifestations– anaphylaxis is a rare but extremely life-threatening systemic type I hypersensitivity reaction. The entry of vasoactive amines into the bloodstream causes contraction of smooth muscle, widespread vasodilation and an increase in vascular permeability with the release of fluid from the vessels into the tissue. The resulting peripheral vascular insufficiency and shock can lead to death within a few minutes (anaphylactic shock). In less severe cases, an increase in vascular permeability leads to allergic edema, which has its most dangerous manifestation in the larynx, because it can cause fatal asphyxia. Systemic anaphylaxis usually occurs following injection of allergens (eg, penicillin, foreign serum, local anesthetics, radiocontrast agents). Less commonly, anaphylaxis can occur when allergens are ingested orally (shellfish, crabs, eggs, berries) or when allergens enter the skin (bee and wasp stings). In sensitized individuals, even small amounts of the allergen can trigger fatal anaphylaxis (eg, intradermal penicillin (penicillin hypersensitivity test)).

HYPERSENSITIVITY TYPE II

Type II hypersensitivity is characterized by the reaction of an antibody with an antigen on the surface of a host cell, which causes the destruction of that cell. The antigen involved may be one's own, but for some reason recognized by the immune system as foreign (an autoimmune disease occurs). The antigen can also be external and can accumulate on the surface of the cell (for example, a drug can be a hapten when it binds to a cell membrane protein and thus stimulates an immune response). As a result of the receipt of the first (“sensitizing”) dose of the antigen, the synthesis of class M and G antibodies with specific reactivity occurs. When the antigen is re-entered, the antigen-antibody reaction occurs on the surface of the cells carrying the antigen, which leads to their lysis, in which several may take part mechanisms. A specific antibody, usually IgG or IgM, produced against an antigen interacts with it on the cell surface and causes cell damage in several ways:

1. Complement-mediated cytotoxicity - activation of the complement cascade leads to the formation of the “membrane attack” complex C5b6789, which causes lysis of the cell membrane.

2. Antibody-dependent cellular cytotoxicity - the antigen-antibody complex is recognized by unsensitized “null” lymphocytes (NK cells), which destroy the cell.

3. Antibody-dependent connective tissue damage – the antibody can bind to connective tissue antigens, thereby causing inflammation.

The manifestations of a type II hypersensitivity reaction depend on the type of cell carrying the antigen. Note that blood transfusion reactions are actually normal immune responses against foreign cells. They are identical in the mechanism of type II hypersensitivity reactions and also adversely affect the patient, and therefore blood transfusion complications are often considered together with disorders that occur with hypersensitivity.

HYPERSENSITIVITY TYPE III

The interaction of antigen and antibody can lead to the formation of immune complexes locally (at the site of damage) or generalized (in the bloodstream). The accumulation of immune complexes in various parts of the body activates complement and causes acute inflammation and necrosis. With type III hypersensitivity, immune complexes accumulate in tissues. This leads to complement activation, which is accompanied by tissue damage and the development of acute inflammation. Immune complex diseases can be systemic, which are caused by circulating antibodies (for example, serum sickness), or local as a result of the formation of immune complexes at the site of antigen entry (Arthus phenomenon).

There are two types of immune complex damage:

Reactions such as the Arthus phenomenon – in reactions such as the Arthus phenomenon, tissue necrosis occurs at the site of antigen injection. Repeated administration of the antigen leads to the accumulation of large amounts of precipitating antibodies in the serum. Subsequent administration of the same antigen leads to the formation of large antigen-antibody complexes, which are deposited locally in small blood vessels, where they activate complement, accompanied by the development of a severe local acute inflammatory reaction with hemorrhage and necrosis. This phenomenon is observed very rarely. It occurs in the skin after repeated administration of the antigen (for example, during rabies vaccination, when multiple injections of the vaccine are given). The severity of inflammation depends on the dose of antigen. Type III hypersensitivity is believed to be responsible for the occurrence of hypersensitivity pneumonitis, a lung disease that presents with cough, dyspnea, and fever 6-8 hours after inhalation of certain antigens. If the supply of antigen is repeated, then chronic granulomatous inflammation occurs. Types I and IV hypersensitivity can coexist with type III.

Reactions such as serum sickness, reactions also caused by immune complex damage, are more common than reactions such as the Arthus phenomenon. The course of reactions depends on the dose of antigen. Repeated intake of a large dose of antigen, for example, foreign serum proteins, drugs, viral and other microbial antigens, leads to the formation of immune complexes in the blood. In the presence of excess antigen, they remain small, soluble, and circulate in the bloodstream. They ultimately pass through the endothelial pores of small vessels and accumulate in the vessel wall, where they activate complement and lead to complement-mediated necrosis and acute inflammation of the vessel wall (necrotizing vasculitis). Vasculitis can be generalized, affecting a large number of organs (for example, in serum sickness due to the introduction of foreign serum or in systemic lupus erythematosus, an autoimmune disease) or can affect a single organ (for example, in post-streptococcal glomerulonephritis). Immune complex damage can occur in many diseases. In some of them, including serum sickness, systemic lupus erythematosus, and poststreptococcal glomerulonephritis, immune complex damage is responsible for the main clinical manifestations of the disease. In others, such as hepatitis B, infective endocarditis, malaria and some types of malignant tumors, immune complex vasculitis occurs as a complication of the disease.

Disease	Cause	Antigen source
Farmer's lungs	Hay dust	Micropolyspora faeni
Bagassoz	Sugar dust	Thermophilic actinomycetes
Pneumonitis from air conditioners	Humidifiers and air conditioners	Thermophilic actinomycetes
Pneumonitis from redwood, maple, cedar	Bark dust, sawdust	Thermophilic actinomycetes, Cryptostroma corticale, sawdust
Mushroom Picker's Lungs	Mushrooms, compost	Thermophilic actinomycetes
Cheesemakers' lungs	Cheese dust	Penicillium casei
Brewers' lungs	Beer dust (yeast)	Aspergillus clavatus
Poultry farmer's lungs	Poultry secretions and serum	Poultry whey proteins
“Enzyme” lungs	Enzyme detergents	Alcalase, obtained from Bacillus subtilis
Drug-induced hypersensitivity pneumonitis	Medicines, industrial materials	Nitrofurantoin, cromolyn, hydrochlorothiazide, etc.
Bath attendant's lungs	Contaminated steam in baths, saunas	Aspergillus pullulans

HYPERSENSITIVITY IV (SLOW) TYPE

Unlike other hypersensitivity reactions, delayed-type hypersensitivity involves cells rather than antibodies. This type is mediated by sensitized T lymphocytes, which either directly exert cytotoxicity or through the secretion of lymphokines. Type IV hypersensitivity reactions typically occur 24 to 72 hours after administration of the antigen to a sensitized individual, distinguishing it from type I hypersensitivity, which often develops within minutes. Histological examination of tissues in which type IV hypersensitivity reaction occurs reveals cell necrosis and pronounced lymphocytic infiltration. Direct cytotoxicity of T cells plays an important role in contact dermatitis, in the response against tumor cells, virus-infected cells, transplanted cells bearing foreign antigens, and in some autoimmune diseases.
T cell hypersensitivity due to the action of various lymphokines also plays a role in granulomatous inflammation, the cause of which is the intracellular persistence of the antigen, which for some reason is not destroyed by macrophages. Long-term cytokine stimulation of macrophages leads to the fusion of the latter and the formation of giant cells. The rate of development of the reaction is about 2 weeks.

The manifestation of this type of hypersensitivity is the basis of skin tests used in the diagnosis of these infections (tuberculin, lepromin, histoplasmin and coccidioidin tests). In these tests, inactivated microbial or fungal antigens are injected intradermally. If the reaction is positive, granulomatous inflammation develops at the injection site within 24–72 hours, which manifests itself as the formation of a papule. A positive test indicates the presence of delayed hypersensitivity to the administered antigen and is evidence that the body has previously been exposed to this antigen.

HYPERSENSITIVITY TYPE V

Antibodies are capable of changing the functional activity of receptors if the receptors are antigens. With the formation of antibodies (IgG) that bind to TSH receptors on the follicular epithelial cells of the thyroid gland, Graves' disease (primary hyperthyroidism) develops. This interaction leads to stimulation of the enzyme adenylate cyclase, which leads to an increase in cAMP levels and to the secretion of increased amounts of thyroid hormones. Inhibitory antibodies play a key role in myasthenia gravis ( myasthenia gravis) is a disease characterized by disruption of neuromuscular transmission and the occurrence of muscle weakness. The disease is caused by antibodies (IgG) directed against acetylcholine receptors on the motor end plate. Antibodies compete with acetylcholine for the binding site on the receptor, thus blocking the transmission of nerve impulses.
The mechanism of inhibition also underlies pernicious anemia, in which antibodies bind to intrinsic factor and inhibit the absorption of vitamin B12.

MORPHOLOGICAL CHANGES IN ORGANS DURING HYPERSENSITIVITY

Morphologically, during antigenic stimulation (sensitization) of the body, the most pronounced changes are observed in the lymph nodes, primarily regional to the site of entry of the antigen. Lymph nodes are enlarged and full of blood. In types I-III of hypersensitivity, an abundance of plasmablasts and plasma cells is detected in the light centers of the follicles of the cortical and in the pulpal cords of the medulla. The number of T-lymphocytes is reduced. A large number of macrophages are noted in the sinuses. The degree of macrophage-plasmacytic transformation of lymphoid tissue reflects the intensity of immunogenesis and, above all, the level of production of antibodies (immunoglobulins) by plasmacytic cells. If, in response to antigenic stimulation, predominantly cellular immune reactions develop (type IV hypersensitivity), then in the lymph nodes in the paracortical zone, mainly sensitized lymphocytes proliferate, rather than plasmablasts and plasma cells. In this case, expansion of T-dependent zones occurs. The spleen enlarges and becomes full of blood. In types I-III of hypersensitivity, sharply enlarged large grayish-pinkish follicles are clearly visible on the section. Microscopically, hyperplasia and plasmatization of the red pulp and an abundance of macrophages are noted. The white pulp, especially along the periphery of the follicles, also contains many plasmablasts and plasmacytes. In type IV hypersensitivity, the morphological changes are similar to the changes observed in the lymph nodes in the T-zones.
In addition, acute immune inflammation occurs in the organs and tissues in which an immediate-type hypersensitivity reaction—HNT (types I, II, III) develops. It is characterized by rapid development, the predominance of alterative and exudative changes. Alternative changes in the form of mucoid, fibrinoid swelling and fibrinoid necrosis are observed in the ground substance and fibrous structures of the connective tissue. In the focus of immune inflammation, plasmorrhagia is expressed, fibrin, neutrophils, and erythrocytes are detected. In type IV hypersensitivity (delayed hypersensitivity reaction - DTH), lymphocytic and macrophage infiltration (sensitized lymphocytes and macrophages) at the site of immune conflict are an expression of chronic immune inflammation. To prove that morphological changes belong to the immune reaction, it is necessary to use an immunohistochemical method; in some cases, electron microscopic examination can help.

AUTOIMMUNE DISEASES.

The immune system recognizes the body's own antigens as “self” antigens and does not react to them (natural tolerance). Autoimmune diseases occur when this natural tolerance is broken, leading to an immune response against self-antigens.
Natural tolerance to antigens occurs when the immune system encounters an antigen in the embryonic period of life. There are central and peripheral tolerance. Central tolerance is a negative selection of autoreactive T- and B-lymphocytes in the central organs of the immune system, i.e. in the thymus and bone marrow (clonal deletion). Peripheral tolerance - at the level of peripheral organs of immunogenesis, is carried out by clonal inactivation of mature T cells and the suppressor effect of T helper cells. Autoimmunization is a breakdown of natural tolerance followed by the emergence of a specific humoral and/or cellular response against the body's own antigens. Cellular damage in autoimmune diseases is caused by both humoral and cellular hypersensitivity (types II, III and IV). There are several different mechanisms for the development of autoimmune diseases.

Mechanisms of development of autoimmune diseases

Mechanisms	Antigens involved in pathogenesis	Reasons for development	Autoimmune diseases
Contact with the immune system of hidden antigens	Thyroglobulin (?)	Normally, thyroglobulin is hidden in the follicles of the thyroid gland	Hashimoto's thyroiditis
Lens proteins	The lens does not have blood vessels; normally the proteins are hidden from the immune system	Sympathetic ophthalmitis
Sperm antigens	Antigens arise in postnatal life	Infertility (in men)
Damage to self antigens	Medicines, viral and other infections	Addition of haptens, partial destruction	Hemolytic anemia, ? systemic lupus erythematosus, ? rheumatic diseases
Decrease in the concentration of suppressor antibodies	Many types	B cell deficiency; Bruton's congenital agammaglobulinemia	Many types
Decrease in the number of T-suppressors	Many types	T-cell deficiency, post-viral infections	Rarely observed
Activation of suppressed lymphocyte clones	Epstein-Barr virus; ? other viruses	B cell stimulation	? Rheumatoid arthritis
The emergence of "forbidden" clones	Many types	Tumor transformation of lymphocytes; malignant lymphoma and lymphocytic leukemia	Hemolytic anemia, thrombocytopenia
Cross immunity to external and self antigens	Antistreptococcal antibodies and myocardial antigens	Antibodies against external antigens act on self-antigens	Rheumatic diseases
Disorders in immune response genes (Ir antigens)	Various types	Loss of control of the immune response due to lack of Ir antigens	Many types 1

1 Immune response genes (Ir antigens) are closely related to HLA antigens. In autoimmune diseases, in which there is damage to Ir antigens, an increase in the prevalence of certain HLA types is determined

The following factors are distinguished in the pathogenesis of autoimmune diseases:

1. Predisposing:

HLA system genes;

Hormonal levels associated with gender;

Genetic determined characteristics of target organ cells.

2. Initiators:

Viral and bacterial infections;

Physical and chemical influences.

3. contributing:

Reduced suppressor activity of T-lymphocytes and anti-idiotypic antibodies.

Related information.

Fungi, protozoa, foreign proteins, transplanted tissues, etc.), however, in some situations the functioning of the immune system is disrupted, which leads to aggression of the body’s own tissues by immune defense factors.

Autoimmune diseases are a group of diseases in which the body’s organs and tissues are destroyed by the body’s own immune system. The most common autoimmune diseases include scleroderma, systemic lupus erythematosus, autoimmune Hashimoto's thyroiditis, diffuse toxic goiter, etc. In addition, the development of many diseases (myocardial infarction, viral hepatitis, streptococcal, herpes, cytomegalovirus infections) can be complicated by the appearance of an autoimmune reaction.

Mechanism of development of autoimmune diseases
The mechanism of development of autoimmune diseases is not fully understood. It is obvious that autoimmune diseases are caused by dysfunction of the immune system as a whole or its individual components.

In particular, it has been proven that suppressor T lymphocytes are involved in the development of systemic lupus erythematosus, myasthenia gravis or diffuse toxic goiter. In these diseases, there is a decrease in the function of this group of lymphocytes, which normally inhibit the development of the immune response and prevent aggression of the body’s own tissues. With scleroderma, there is an increase in the function of helper T-lymphocytes (T-helpers), which in turn leads to the development of an excessive immune response to the body’s own antigens. It is possible that both of these mechanisms, as well as other types of dysfunction of the immune system, are involved in the pathogenesis of some autoimmune diseases. The functionality of the immune system is largely determined by hereditary factors, which is why many autoimmune diseases are passed on from generation to generation. The function of the immune system may be impaired under the influence of external factors such as infections, injuries, stress. At the moment, it is believed that unfavorable external factors, as such, are not capable of causing the development of an autoimmune disease, but only increase the risk of its development in individuals with a hereditary predisposition to this type of pathology.

Classic autoimmune diseases are relatively rare. Autoimmune complications of certain diseases occur much more often. The addition of an autoimmune mechanism can greatly aggravate the evolution of the disease and therefore determines the prognosis of the disease. Autoimmune reactions occur, for example, with burns, chronic sore throats, myocardial infarction, viral diseases, and injuries to internal organs. The pathogenesis of the development of autoimmune reactions is very complex and largely unclear. At the moment, it is reliably known that some organs and tissues of the human body develop in relative isolation from the immune system, therefore, at the time of differentiation of immune cells, clones capable of attacking these types of tissues or organs are not removed. Autoimmune aggression occurs when, for some reason, the barrier separating these tissues or organs from the immune system is destroyed and they are recognized by immune cells as “foreign.” This happens to the tissues of the eye or testicle, which can undergo an autoimmune attack during various inflammatory reactions (during inflammation, tissue barriers are broken). Another mechanism for the development of autoimmune diseases is cross-immune reactions. It is known that some bacteria and viruses, as well as some drugs, are similar in structure to some components of human tissue. During an infectious disease caused by a given type of bacteria or virus, or while taking a certain medication, the immune system begins to produce antibodies that are able to react with normal body tissues that have components similar to the antigens that caused the immune response. The mechanism described above underlies the occurrence of rheumatism (cross-reaction to streptococcal antigens), diabetes mellitus (cross-reaction to antigens of the Coxsackie B virus and hepatitis A), hemolytic anemia (cross-reaction to medications).

During various diseases, body tissues undergo partial denaturation (change in structure), which gives them the properties of foreign structures. In such cases, autoimmune reactions may occur that are directed against healthy tissue. This mechanism is typical for skin damage due to burns, Dresler syndrome (pericarditis, pleurisy) during myocardial infarction. In other cases, healthy tissues of the body become a target for the body's own immune system due to the attachment of a foreign antigen to them (for example, with viral hepatitis B).

Another mechanism of autoimmune damage to healthy tissues and organs is their involvement in allergic reactions. A disease such as glomerulonephritis (damage to the glomerular apparatus of the kidneys) develops as a result of the deposition in the kidneys of circulating immune complexes that are formed during a common sore throat.

Evolution of autoimmune diseases
The evolution of autoimmune diseases depends on the type of disease and the mechanism of its occurrence. Most true autoimmune diseases are chronic. Their development is marked by periods of exacerbations and remissions. As a rule, chronic autoimmune diseases lead to serious dysfunction of internal organs and disability of the patient. Autoimmune reactions that accompany various diseases or the use of medications, on the contrary, are short-lived and disappear along with the disease that caused their development. In some cases, the consequences of autoimmune aggression of the body can give rise to an independent pathology of a chronic nature (for example, type 1 diabetes after a viral infection).

Diagnosis of autoimmune diseases
Diagnosis of autoimmune diseases is based on determining the immune factor that causes damage to organs and tissues of the body. Such specific factors have been identified for most autoimmune diseases.

For example, in the diagnosis of rheumatism, rheumatoid factor is determined, in the diagnosis of systemic lupus - LES cells, anti-nucleus antibodies (ANA) and anti-DNA, scleroderma antibodies Scl-70. To determine these markers, various laboratory immunological research methods are used.

The clinical progression of the disease and symptoms of the disease can provide useful information for establishing the diagnosis of an autoimmune disease.

The development of scleroderma is characterized by skin damage (foci of limited edema, which slowly undergo compaction and atrophy, the formation of wrinkles around the eyes, smoothing of the skin texture), damage to the esophagus with impaired swallowing, thinning of the terminal phalanges of the fingers, diffuse damage to the lungs, heart and kidneys. Lupus erythematosus is characterized by the appearance on the skin of the face (on the back of the nose and under the eyes) of a specific redness in the form of a butterfly, damage to the joints, the presence of anemia and thrombocytopenia. Rheumatism is characterized by the appearance of arthritis after a sore throat and the later formation of defects in the valvular apparatus of the heart.

Treatment of autoimmune diseases
Recently, significant advances have been made in the treatment of autoimmune diseases. Taking into account the fact that the main factor damaging the body’s tissues is the body’s own immune system, treatment for autoimmune diseases is immunosuppressive and immunomodulatory in nature.

Immunosuppressants This is a group of drugs that suppress the function of the immune system. These substances include cytostatics (Azathioprine, Cyclophosphamide), corticosteroid hormones (Prednisolone, Dexamethasone), antimetabolites (Mercaptopurine), some types of antibiotics (Tacrolimus), antimalarials (Quinine), 5-aminosalicylic acid derivatives, etc. The general characteristic of these drugs is suppression of immune system function and reduction in the intensity of inflammatory reactions.

With long-term use of these drugs, serious adverse reactions may develop, such as, for example, inhibition of hematopoiesis, infections, liver or kidney damage. Some of these drugs inhibit cell division in the body and therefore can cause side effects such as hair loss. Hormonal drugs (Prednisolone, Dexamethasone) can cause the development of Cushing's syndrome (obesity, high blood pressure, gynecomastia in men). These drugs can only be prescribed by a qualified specialist and only after an accurate diagnosis has been established.

Immunomodulatory agents used to restore balance between various components of the immune system. At the moment, there are no specific immunomodulatory agents recommended for etiotropic or pathogenetic treatment of autoimmune diseases. On the other hand, immunostimulating drugs are very useful for the prevention and treatment of infectious complications that arise from the use of immunosuppressants, discussed above.

Alfetin– a drug containing a protein similar to fetal albumin, has a pronounced immunomodulatory effect by increasing the secretion of biologically active substances that regulate the function of T-lymphocytes. Taking Alfetin reduces the need for corticosteroid drugs. The drug itself is non-toxic and is well tolerated by the body.

Preparations of Echinacea purpurea, Rhodiola rosea, and Ginseng extract are used as immunomodulators.

Due to the fact that most autoimmune diseases occur against the background of vitamin and mineral deficiency, their complex treatment in most cases is supplemented with complexes of vitamins and minerals, as well as various nutritional supplements rich in these elements.

The use of immunomodulatory drugs should be agreed with the attending physician. In the case of some autoimmune diseases, immunomodulators are contraindicated.

Bibliography:

Zemskov A.M., Immunopathology, allergology, infectology, 2000
Kozlov V.A. Immunotherapy of allergic, autoimmune and other diseases, Novosibirsk: Agro-Sibir, 2004
Modern problems of allergology, immunology and immunopharmacology, M., 2002

The site provides reference information for informational purposes only. Diagnosis and treatment of diseases must be carried out under the supervision of a specialist. All drugs have contraindications. Consultation with a specialist is required!

Autoimmune diseases– these are human diseases that manifest themselves as a consequence of too high activity of the body’s immune system relative to its own cells. The immune system perceives its tissues as foreign elements and begins to damage them. Such diseases are also called systemic, since a certain system of the body as a whole is affected, and sometimes the entire body is affected.

For modern doctors, the causes and mechanism of manifestation of such processes remain unclear. Thus, there is an opinion that autoimmune diseases can be triggered by stress, trauma, infections of various kinds, and hypothermia.

Among the diseases that belong to this group of ailments, it should be noted , a number of autoimmune thyroid diseases. The mechanism of development is also autoimmune first type, multiple sclerosis , . There are also some syndromes that are autoimmune in nature.

Causes of autoimmune diseases

The human immune system matures most intensively from birth to the age of fifteen. During the process of maturation, cells subsequently acquire the ability to recognize certain proteins of foreign origin, which becomes the basis for fighting various infections.

Autoimmune thyroiditis

Autoimmune This is the most common type of thyroiditis. Experts distinguish two forms of this disease: atrophic thyroiditis and hypertrophic thyroiditis (called Hashimoto's goiter ).

Autoimmune thyroiditis is characterized by the presence of both qualitative and quantitative deficiency of T-lymphocytes. Symptoms of autoimmune thyroiditis are manifested by lymphoid infiltration of the thyroid tissue. This condition manifests itself as a consequence of the influence of autoimmune factors.

Autoimmune thyroiditis develops in people who have a hereditary tendency to this disease. Moreover, it manifests itself under the influence of a number of external factors. The consequence of such changes in the thyroid gland is the subsequent occurrence of secondary autoimmune hypothyroidism.

In the hypertrophic form of the disease, the symptoms of autoimmune thyroiditis are manifested by a general enlargement of the thyroid gland. This increase can be determined both by palpation and visually. Very often, the diagnosis of patients with a similar pathology will be nodular goiter.

In the atrophic form of autoimmune thyroiditis, the clinical picture of hypothyroidism most often occurs. The end result of autoimmune thyroiditis is autoimmune hypothyroidism, in which there are no thyroid cells at all. Symptoms of hyperthyroidism include trembling fingers, heavy sweating, increased heart rate, and increased blood pressure. But the development of autoimmune hypothyroidism occurs several years after the onset of thyroiditis.

Sometimes there are cases of thyroiditis without specific symptoms. But still, in most cases, early signs of this condition are often a certain discomfort in the thyroid gland. During the process of swallowing, the patient may constantly feel a lump in the throat, a feeling of pressure. During palpation, the thyroid gland may hurt a little.

Subsequent clinical symptoms of autoimmune thyroiditis in humans are manifested by coarsening of facial features, bradycardia , the appearance . The patient's voice changes, memory and speech become less clear, and shortness of breath appears during physical activity. The condition of the skin also changes: it thickens, dry skin occurs. Women note a violation of the monthly cycle; often develops against the background of autoimmune thyroiditis . Despite such a wide range of symptoms of the disease, it is almost always difficult to diagnose. In the process of establishing a diagnosis, palpation of the thyroid gland and a thorough examination of the neck area are often used. It is also important to determine the level of thyroid hormones and determine antibodies in the blood. If absolutely necessary, an ultrasound of the thyroid gland is performed.

Treatment of autoimmune thyroiditis is usually carried out with the help of conservative therapy, which involves the treatment of various disorders of the thyroid gland. In especially severe cases, autoimmune treatment is carried out surgically using the method thyroidectomy .

If the patient exhibits hypothyroidism, treatment is carried out using replacement therapy, for which thyroid preparations of thyroid hormones are used.

Autoimmune hepatitis

Reasons why a person develops autoimmune hepatitis, are not completely known to this day. There is an opinion that autoimmune processes in the patient’s liver are provoked by various viruses, for example, hepatitis viruses of various groups , , herpes virus. Autoimmune hepatitis most often affects girls and young women; in men and older women the disease is much less common.

Autoimmune hepatitis is progressive in nature, with relapses of the disease occurring very often. A patient with this disease experiences very severe liver damage. Symptoms of autoimmune hepatitis are jaundice, increased body temperature, and pain in the liver area. Hemorrhages appear on the skin. Such hemorrhages can be either small or quite large. Also, in the process of diagnosing the disease, doctors discover an enlarged liver and spleen.

As the disease progresses, changes are also observed in other organs. Patients experience enlargement of the lymph nodes and pain in the joints. Later, severe damage to the joint may develop, causing swelling. It is also possible to develop rashes, focal scleroderma, and psoriasis. The patient may suffer from muscle pain, sometimes damage to the kidneys, heart, and the development of myocarditis occurs.

During the diagnosis of the disease, a blood test is performed, in which there is an increase in liver enzymes, the level is too high , increase in thymol test, disturbance in the content of protein fractions. The analysis also reveals changes that are characteristic of inflammation. However, markers of viral hepatitis are not detected.

Corticosteroid hormones are used in the treatment of this disease. At the first stage of therapy, very high doses of such drugs are prescribed. Later, over several years, maintenance doses of such medications should be taken.