What diseases are autoimmune? Autoimmune disease

It's no secret that the human immune system is aimed at protecting the body's organs and cells from the negative effects of viruses, bacteria and infections. As a result of exposure to both internal and external factors, the functioning of the immune system is disrupted, and its system begins to perceive its own tissues, organs and cells as foreign.

At this moment, an irreparable process begins, aimed at destruction, and subsequently death of the body. How to prevent autoimmune diseases in time? And what should you do if your immune system has already taken the path of destruction?

Autoimmune diseases are diseases whose development and formation are associated with a complete disruption of the immune system. These diseases are usually called systemic. After all, starting with the destruction of one organ or tissue, the process of damage to the entire organism begins.

The most common autoimmune diseases today: AIDS, SARS, Graves' disease or diffuse toxic goiter, Hashimoto's thyroiditis, systemic lupus erythematosus, type 1 diabetes, multiple sclerosis, avian influenza, rheumatoid arthritis, scleroderma, vitiligo, Sjögren's syndrome, Crohn's disease . The worst thing is that this is not the entire list of autoimmune diseases that affect the human body.

Despite the fact that the first autoimmune disease was diagnosed more than 100 years ago, the mechanism of development and causes of the disease have not been thoroughly studied. What is known is that diseases are a direct result of impaired functionality of the human immune system. The symptoms of the disease are also not fully defined. In some cases, a person may not even be aware of the presence of the disease.

It has been proven that suppressor T lymphocytes are involved in the development of systemic lupus erythematosus, as well as Graves' disease. Their main function is to regulate the immune response to viruses and bacteria entering the body. In an autoimmune disease, T lymphocytes do not respond to immune damage, and in some cases their action is completely blocked.

As a rule, the functioning of the human immune system is determined by genetic factors. This means that autoimmune diseases of the thyroid gland, scleroderma, rheumatoid arthritis - could be in one of your direct relatives.

Causes of diseases

The human immune system is formed in the first year of life and finally matures in the period from 13 to 15 years. It is at this moment that the body’s autoimmune reaction to viruses, foreign proteins and infections begins. It is worth noting that during the maturation of the immune system, most T-lymphocytes begin to perceive the protein contained in human blood as a foreign object.

This immune response is necessary to suppress and destroy damaged cells throughout life. But, at some stage, the control of the immune system over such a reaction of T-lymphocytes is blocked as a result of unknown reasons. As a result, human immunodeficiency disease begins to develop, because T-lymphocytes begin to completely destroy healthy cells.

At the moment, such damage to the immune system is usually classified according to the reasons for its formation. They can be external and internal.

External causes include infections that provoke diseases and adverse environmental effects (radiation, toxic emissions, exposure to ultraviolet radiation). Autoimmune diseases that occur as a result of an infection or virus entering the body are characterized by changes in the chemical and molecular composition of body tissues.

Consequently, the autoimmune process starts, and immune cells attack the organ tissue, destroying them as foreign. Afterwards, the inflammatory process develops and the total destruction of the entire organism begins. This autoimmune reaction of the body occurs as a result of cell damage by the human immunodeficiency virus (HIV).

Internal causes include hereditary factors accompanied by gene mutations. This category includes autoimmune thyroid diseases.

Pathological diseases of the thyroid gland

Autoimmune disease of the thyroid gland - this diagnosis is heard by every seventh person on the planet. The thyroid gland is the engine of the body, thanks to which it produces hormones necessary for the life and functioning of all human organs and systems.

Autoimmune thyroid diseases can be divided into two categories.

1. Graves' disease or diffuse toxic goiter of the thyroid gland, characterized by the release of excess amounts of hormones.
2. Hashimoto's thyroiditis, which is accompanied by hormonal deficiency - hypothyroidism.

Symptoms of Graves' disease manifest themselves in the form of sudden weight loss that cannot be controlled by diet. The patient has a violation of blood pressure, an increase in body temperature for no apparent reason, as well as disturbances in the functioning of the gastrointestinal tract. Symptoms that are typical for women are menstrual irregularities and lack of ovulation. In men, Basedow's disease causes a decrease in potency and sperm production.

The causes of Graves' disease or thyrotoxicosis can be diffuse toxic goiter, multinodular goiter, thyroid cancer, autoimmune thyroiditis.

Treatment methods for Graves' disease

Treatment for autoimmune diseases depends on the nature of the disease and the complications it causes. There are 3 methods of treating Graves' disease that are widely practiced at the moment.

Drug treatment. This type of treatment is based on long-term hormonal therapy with thyreostatic drugs. As a rule, these are medications containing radioactive iodine, which is aimed at destroying affected thyroid cells. Hormonal therapy in this case will be aimed at maintaining the functioning of those organs whose work depended on thyroid hormones. These are the cardiovascular and central nervous systems.

Surgical intervention. Autoimmune disease of the thyroid gland - Graves' disease is eliminated surgically if drug treatment with radioactive iodine has not brought results. Surgery is also necessary if the patient has symptoms of cancer of the thyroid tissue. In this case, it is recommended to remove the gland node or the entire goiter, depending on the location of the cancer.

Radiation therapy is used in late stage thyroid cancer.

Hashimoto's goiter - causes of formation and treatment

Hashimoto's goiter or lymphotous goiter is a disease of the thyroid gland, manifested in the form of an inflammatory process of tissues. As a rule, goiter is accompanied by hypothyroidism (hormonal deficiency) and gradual atrophy of gland tissue.

Symptoms of Hashimoto's goiter manifest themselves in the form of general weakness of the body, fatigue, and increased fatigue. If the goiter has undergone diffuse changes and increased in size, then the person begins to feel severe pain in the neck and chest. This is caused by the fact that the thyroid gland, growing, begins to put pressure on neighboring organs - the upper respiratory tract and nerve endings.

Risk factors include patients who are currently diagnosed with diffusion goiter of the thyroid gland, as well as those who have undergone any surgical interventions in the endocrine system. In this case, we should not forget about the hereditary factor.

Treatment of autoimmune diseases of this type does not have a specific focus. Hashimoto's goiter is suppressed with hormonal therapy over several years. The goal of this treatment is to reduce the size of the thyroid gland and block the pituitary gland, which stimulates the production of thyroid hormones in excess quantities. If the goiter tissue is compacted and at risk of forming a cancerous tumor, then surgical intervention will be necessary.

Advances in the treatment of autoimmune diseases

Medicine does not stand still, so at the moment autoimmune diseases are treated with the help of immunosuppressive substances. These are substances that can block the function of the immune system and reduce the inflammatory process in body tissues.

But, a significant disadvantage of such drugs is the side effects that appear after their use. Symptoms such as hair loss, bleeding disorders, obesity, increased blood pressure and gynecomastia in men (breast formation) are typical after taking medications.

Autoimmune diseases are treated with drugs such as azathioprine, cyclophosphamide, dexamethasone, quinine, tacrolimus. It is necessary to understand that self-prescription of the above drugs can lead to irreversible consequences. Be sure to contact a medical facility for professional advice. If you find any symptoms, then you should not waste time, because it is better to prevent the disease than to treat it later for more than one month or even a year.

Autoimmune diseases are diseases that develop when the body's immune system becomes overly sensitive for any reason. Normally, the work of the immune system is to protect and protect the human body from various kinds of antigens and external factors that harm it. However, under certain conditions, this system begins to function incorrectly and becomes hypersensitive. It begins to overreact to external conditions that are otherwise normal, and over time causes the development of various diseases.

One of the symptoms of an autoimmune disease is sudden hair loss

Autoimmune diseases- These are diseases that the human body develops on its own. They can be either genetic or acquired, and are not only a problem for adults - their symptoms are also found in children. People with such diseases need to be very careful about their lifestyle. The following list includes many autoimmune diseases, but there are others that are still being researched to understand their causes and therefore remain on the list of suspected autoimmune diseases.

The symptoms of autoimmune diseases are numerous. They include a wide variety of manifestations (ranging from headaches to skin rashes) that affect almost all body systems. There are many of them, since the number of autoimmune diseases themselves is large. Below is a list of these symptoms, covering almost all autoimmune diseases along with their common signs.

After reviewing this list, it becomes clear that even a simple health problem can be a sign of an autoimmune disease. A number of autoimmune diseases have already been studied, and the symptoms associated with them have been described. However, there are many other diseases that are still waiting to be included in the above list. Thus, the list of autoimmune diseases continues to grow daily, and the number of their symptoms increases exponentially. As can be seen from the table, one symptom can be common to various diseases, so diagnosis based only on symptoms is difficult. In this regard, instead of assuming that you have any of the listed diseases, it is recommended to consult a doctor and begin treatment aimed at eliminating/controlling the existing symptoms.

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AUTOIMMUNE DISEASES AND DISEASES OF IMMUNE COMPLEXES

AUTOIMMUNE DISEASES

Autoimmune diseases are quite widespread in the human population: they affect up to 5% of the world's population. For example, 6.5 million people in the United States suffer from rheumatoid arthritis; in large cities in England, up to 1% of adults are disabled with multiple sclerosis; juvenile diabetes affects up to 0.5% of the world's population. The sad examples can be continued.

First of all, it should be noted the difference between autoimmune reactions, or autoimmune syndrome And autoimmune diseases, which are based on the interaction between the components of the immune system and one’s own healthy cells and tissues. The former develop in a healthy body, proceed continuously and eliminate dying, aging, diseased cells, and also arise in any pathology, where they act not as its cause, but as a consequence. Autoimmune diseases, of which there are currently about 80, are characterized by a self-sustaining immune response to the body’s own antigens, which damages cells containing self-antigens. Often the development of an autoimmune syndrome further develops into an autoimmune disease.

Classification of autoimmune diseases

Autoimmune diseases are conventionally divided into three main types.

1. Organ-specific diseases, which are caused by autoantibodies and sensitized lymphocytes against one or a group of autoantigens of a specific organ. Most often, these are barrier antigens to which there is no natural (innate) tolerance. These include Hoshimoto's thyroiditis, myasthenia gravis, primary myxedema (thyrotoxicosis), pernicious anemia, autoimmune atrophic gastritis, Addison's disease, early menopause, male infertility, pemphigus vulgaris, sympathetic ophthalmia, autoimmune myocarditis and uveitis.

2. For non-organ-specific diseases autoantibodies to autoantigens of cell nuclei, cytoplasmic enzymes, mitochondria, etc. interact with different tissues of a given or even another

type of organism. In this case, autoantigens are not isolated (are not “barrier”) from contact with lymphoid cells. Autoimmunization develops against the background of pre-existing tolerance. Such pathological processes include systemic lupus erythematosus, discoid erythematous lupus, rheumatoid arthritis, dermatomyositis (scleroderma).

3. Mixed diseases involve both of these mechanisms. If the role of autoantibodies is proven, then they should be cytotoxic against the cells of the affected organs (or act directly through the AG-AT complex), which, when deposited in the body, cause its pathology. These diseases include primary biliary cirrhosis, Sjögren's syndrome, ulcerative colitis, celiac enteropathy, Goodpasture's syndrome, type 1 diabetes mellitus, and an autoimmune form of bronchial asthma.

Mechanisms of development of autoimmune reactions

One of the main mechanisms that prevents the development of autoimmune aggression in the body against its own tissues is the formation of unresponsiveness to them, called immunological tolerance. It is not congenital, it is formed in the embryonic period and consists of negative selection, those. elimination of autoreactive cell clones that carry autoantigens on their surface. It is the violation of such tolerance that is accompanied by the development of autoimmune aggression and, as a consequence, the formation of autoimmunity. As Burnet noted in his theory, during the embryonic period, contact of such autoreactive clones with “their” antigen causes not activation, but cell death.

However, not all so simple.

Firstly, it is important to say that the antigen recognition repertoire located on T lymphocytes preserves all clones of cells carrying all types of receptors for all possible antigens, including autoantigens, on which they are complexed together with their own HLA molecules, which makes it possible to distinguish “own” and “foreign” cells. This is the stage of "positive selection" followed by negative selection autoreactive clones. They begin to interact with dendritic cells carrying the same complexes of HLA molecules with thymic autoantigens. This interaction is accompanied by signal transmission to autoreactive thymocytes, and they undergo death through the mechanism of apoptosis. However, not all autoantigens are present in the thymus, so some

autoreactive T cells are still not eliminated and move from the thymus to the periphery. They are the ones who provide the autoimmune “noise.” However, as a rule, these cells have reduced functional activity and do not cause pathological reactions, just like autoreactive B lymphocytes, which are subject to negative selection and escape elimination, also cannot cause a full autoimmune response, since they do not receive a costimulatory signal from T helper cells, and in addition, they can be suppressed by special suppressor drugs veto -cells.

Secondly, despite negative selection in the thymus, some autoreactive lymphocyte clones still survive due to the imperfection of the elimination system and the presence of long-term memory cells, circulate in the body for a long time and cause the subsequent development of autoimmune aggression.

After the creation of Erne's new theory in the 70s of the last century, the mechanisms of development of autoimmune aggression became even more clear. It was assumed that the body constantly operates a system self-control including the presence on lymphocytes of receptors for antigens and special receptors for these receptors. Such antigen-recognizing receptors and antibodies to antigens (which are also actually their soluble receptors) were called idiots, and the corresponding antireceptors, or antiantibodies - anti-idiotypes.

Currently the balance between idiotype-antiidiotype interactions is considered as the most important self-recognition system, which is a key process in maintaining cellular homeostasis in the body. Naturally, a violation of this balance is accompanied by the development of autoimmune pathology.

Such a disorder may be caused by: (1) a decrease in the suppressor activity of cells, (2) the appearance in the bloodstream of barrier (“sequestered” antigens of the eye, gonads, brain, cranial nerves, with which the immune system normally does not have contact and when it occurs reacts to them as foreign, (3) antigenic mimicry due to microbial antigens that have common determinants with normal antigens, (4) mutation of autoantigens, accompanied by modification of their specificity, (5) increase in the number of autoantigens in circulation, (6) modification of autoantigens by chemical agents, viruses, etc. with the formation of biologically highly active superantigens.

The key cell of the immune system in the development of autoimmune diseases is the autoreactive T-lymphocyte, which reacts to a specific autoantigen in organ-specific diseases and then, through the immune cascade and the involvement of B-lymphocytes, causes the formation of organ-specific autoantibodies. In the case of organ-nonspecific diseases, most likely, autoreactive T lymphocytes interact not with the epitope of the autoantigen, but with the antigenic determinant of anti-idiotypic autoantibodies to it, as indicated above. Moreover, autoreactive B lymphocytes, which cannot be activated in the absence of a T cell costimulatory factor and synthesize autoantibodies, themselves have the ability to present a mimic antigen without an Ag-presenting cell and present it to non-autoreactive T lymphocytes, which turn into T helper cells and activate B cells for the synthesis of autoantibodies.

Among the autoantibodies produced by B lymphocytes, the following are of particular interest: natural autoantibodies to autologous antigens, which in a significant percentage of cases are detected and persist for a long time in healthy people. As a rule, these are autoantibodies of the IgM class, which, apparently, should still be considered precursors of autoimmune pathology. For this reason, in order to understand the detailed situation and establish the pathogenic role of autoantibodies, the following criteria for diagnosing autoaggression are proposed:

1. Direct evidence of circulating or associated autoAbs or sensitized Lf directed against autoAgs associated with the disease.

2. Identification of the causative autoAG against which the immune response is directed.

3. Adoptive transfer of the autoimmune process by serum or sensitized Lf.

4. The possibility of creating an experimental model of the disease with morphological changes and the synthesis of AT or sensitized Lf when modeling the disease.

Be that as it may, specific autoantibodies serve as markers of autoimmune diseases and are used in their diagnosis.

It should be noted that the presence of specific autoantibodies and sensitized cells is not yet sufficient for the development of an autoimmune disease. A major role is played by pathogenic environmental factors (radiation, force fields, polluted

products, microorganisms and viruses, etc.), genetic predisposition of the body, including those linked to HLA genes (multiple sclerosis, diabetes, etc.), hormonal levels, use of various medications, immune disorders, including cytokine balance.

At present, a number of hypotheses for the mechanism of induction of autoimmune reactions can be proposed (the information given below is partially borrowed from R.V. Petrov).

1. Despite the self-control system, the body contains autoreactive T- and B-lymphocytes, which, under certain conditions, interact with antigens of normal tissues, destroy them, promoting the release of hidden autoantigens, stimulants, mitogens that activate cells, including B-lymphocytes.

2. For injuries, infections, degenerations, inflammation, etc. “sequestered” (barrier) autoantigens are released, to which autoantibodies are produced that destroy organs and tissues.

3. Cross-reacting “mimicking” antigens of microorganisms, common with autoantigens of normal tissues. Staying in the body for a long time, they eliminate tolerance and activate B cells to synthesize aggressive autoantibodies: for example, group A hemolytic streptococcus and rheumatic disease of the heart valves and joints.

4. “Superantigens” - toxic proteins formed by cocci and retroviruses that cause strong activation of lymphocytes. For example, normal antigens activate only 1 in 10,000 T cells, and superantigens activate 4 out of 5! The autoreactive lymphocytes present in the body will immediately trigger autoimmune reactions.

5. The presence in patients of a genetically programmed weakness of the immune response to a specific antigen immunodeficiency. If it is contained by a microorganism, a chronic infection occurs, destroying tissue and releasing various autoags, to which an autoimmune response develops.

6. Congenital deficiency of T-suppressor cells, which abolishes the control of B-cell function and induces their response to normal antigens with all the consequences.

7. Autoantibodies under certain conditions “blind” Lf, blocking their receptors that recognize “self” and “foreign”. As a result, natural tolerance is canceled and an autoimmune process is formed.

In addition to the above mechanisms of induction of autoimmune reactions, it should also be noted:

1. Induction of the expression of HLA-DR antigens on cells that previously did not have them.

2. Induction by viruses and other agents of modification of the activity of autoantigens-oncogenes, regulators of cytokine production and their receptors.

3. Reduced apoptosis of T-helper cells that activate B-lymphocytes. Moreover, in the absence of a proliferative stimulus, B lymphocytes die from apoptosis, whereas in autoimmune diseases it is suppressed and such cells, on the contrary, accumulate in the body.

4. Mutation of the Fas ligand, which leads to the fact that its interaction with the Fas receptor does not induce apoptosis in autoreactive T cells, but suppresses the binding of the receptor to the soluble Fas ligand and thereby delays the cell apoptosis induced by it.

5. Deficiency of special T-regulatory CD4+CD25+ T-lymphocytes with FoxP3 gene expression, which block the proliferation of autoreactive T-lymphocytes, which significantly enhances it.

6. Disruption of the binding site on chromosomes 2 and 17 of the special regulatory protein Runx-1 (RA, SLE, psoriasis).

7. Formation in the fetus of autoantibodies of the IgM class to many components of autocells, which are not eliminated from the body, accumulate with age and cause autoimmune diseases in adults.

8. Immune drugs, vaccines, immunoglobulins can cause autoimmune disorders (dopegite - hemolytic anemia, apressin - SLE, sulfonamides - periarteritis nodosa, pyrazolone and its derivatives - agranulocytosis).

A number of drugs can, if not induce, then intensify the onset of immunopathology.

It is very important for physicians to know that the following drugs have immunostimulating potencies: antibiotics(Eric, amphotericin B, levorin, nystatin),nitrofurans(furazolidone),antiseptics(chlorophyllipt),metabolism stimulants(orotate K, riboxin),psychotropic drugs(nootropil, piracetam, phenamine, sydnocarb),plasma replacement solutions(hemodez, rheopolyglucin, gelatinol).

The association of autoimmune diseases with other diseases

Autoimmune disorders (rheumatic diseases) may be accompanied by tumor lesions of lymphoid tissue and neoplastic

lasers of other localizations, but patients with lymphoproliferative diseases often exhibit symptoms of autoimmune conditions (Table 1).

Table 1. Rheumatic autoimmune pathology in malignant neoplasms

Thus, with hypertrophic osteoarthropathy, cancer of the lungs, pleura, diaphragm, and less often of the gastrointestinal tract is detected, with secondary gout - lymphoproliferative tumors and metastases, with pyrophosphate arthropathy and monoarthritis - bone metastases. Often polyarthritis and lupus-like and scleral-like syndromes are accompanied by malignant tumors of various localizations, and polymyalgia rheumatica and cryoglobulinemia are accompanied, respectively, by cancer of the lungs, bronchi and hyperviscosity syndrome.

Often malignant neoplasms are manifested by rheumatic diseases (Table 2).

With rheumatoid arthritis, the risk of developing lymphogranulomatosis, chronic myeloid leukemia, and myeloma is increased. Tumors more often occur during the chronic course of the disease. The induction of neoplasms increases with the duration of the disease, for example, in Sjögren's syndrome, the risk of cancer increases by 40 times.

These processes are based on the following mechanisms: expression of the CD5 antigen on B cells that synthesize organ-specific antibodies (normally this antigen is presented on T lymphocytes); excessive proliferation of large granular lymphocytes, having

Table 2. Malignant tumors and rheumatic diseases

those with the activity of natural killer cells (phenotypically they belong to CD8 + lymphocytes); infection with retroviruses HTLV-1 and Epstein-Barr viruses; polyclonal activation of B cells with loss of regulation of this process; hyperproduction of IL-6; long-term treatment with cytostatics; disruption of natural killer cell activity; deficiency of CD4+ lymphocytes.

In primary immunodeficiencies, signs of autoimmune processes are often found. A high frequency of autoimmune disorders has been identified in sex-linked hypogammaglobulinemia, IgA deficiency, immunodeficiency with overproduction of IgA, ataxia-telangiectasia, thymoma, and Wiskott-Aldrich syndrome.

On the other hand, there are a number of autoimmune diseases in which immunodeficiencies have been identified (primarily related to T-cell function). In persons with systemic diseases, this phenomenon is expressed more often (with SLE in 50-90% of cases) than with organ-specific diseases (with thyroiditis in 20-40% of cases).

Autoantibodies occur more often in older people. This applies to the determination of rheumatoid and antinuclear factors, as well as antibodies detected in the Wasserman reaction. In asymptomatic 70-year-olds, autoantibodies against various tissues and cells are detected in at least 60% of cases.

What is common in the clinical picture of autoimmune diseases is their duration. There are chronic progressive or chronically relapsing course of pathological processes. Information about the features of the clinical expression of individual autoimmune diseases is presented below (partial information provided is borrowed from S.V. Suchkov).

Characteristics of some autoimmune diseases

Systemic lupus erythematosus

An autoimmune disease with systemic damage to connective tissue, with collagen deposition and the formation of vasculitis. It is characterized by polysymptoms and usually develops in young people. Almost all organs and many joints are involved in the process, and kidney damage is fatal.

With this pathology, antinuclear autoantibodies are formed to DNA, including native DNA, nucleoproteins, cytoplasmic and cytoskeletal antigens, and microbial proteins. It is believed that autoAbs to DNA appear as a result of the formation of its immunogenic form in complex with a protein, or an IgM autoantibody of anti-DNA specificity, which arose in the embryonic period, or the interaction of idiotype-antiidiotype and cell components during microbial or viral infection. Perhaps a certain role belongs to cell apoptosis, which in SLE causes, under the influence of caspase 3, the cleavage of the nucleoproteasome complex of the nucleus with the formation of a number of products that react with the corresponding autoantibodies. Indeed, the content of nucleosomes is sharply increased in the blood of patients with SLE. Moreover, autoantibodies to native DNA are the most diagnostically significant.

An extremely interesting observation is the discovery that DNA-binding autoantibodies also have the enzymatic ability to hydrolyze a DNA molecule without complement. This antibody was called a DNA abzyme. There is no doubt that this fundamental pattern, which, as it turns out, is realized not only in SLE, plays a huge role in the pathogenesis of autoimmune diseases. In this model, the anti-DNA autoantibody has cytotoxic activity towards the cell, which is realized by two mechanisms: receptor-mediated apoptosis and DNA abzyme catalysis.

Autoimmune diseases (AI) are a group of diseases in which the body’s tissues are destroyed by the body’s own immune system (Greek Autos - itself, Immunitas - to free, to protect). The reasons for this mechanism are not fully understood. The list of human autoimmune diseases includes about 140 pathologies, but this is clearly inconclusive data. Over time, many diseases of unknown etiology are increasingly identified as autoimmune.

Briefly about immunity

Yes, there is a constant war going on within us. And we are protected by a powerful army called the immune system. It is very complex, formed in the process of evolution, is constantly being improved and is truly a reliable protector. When a foreign agent enters the body, immune cells destroy it either directly or indirectly by producing antibodies. In the same way, the immune system fights foreign tissues (transplanted from donors), as well as cancerous tumors.

But just as the most perfect computer system has glitches, the immune system is not always perfect. Scientists have not yet figured out the exact reason why our defense makes errors. But the fact has been proven: sometimes immune cells mistake their own cells for foreign ones and begin to destroy them. This is how AIs develop.

How do autoimmune diseases develop?

It is believed that every person has autoreactive lymphocytes that can attack their own cells. But they are blocked by the same immune system (T-suppressors), and if their quantity is small, they are harmless to the body. But sometimes a mechanism is triggered when T-suppressors are unable to restrain the proliferation of such cells. This process of self-aggression usually cannot be stopped by anything.

In most cases, an autoimmune disease occurs suddenly, and the exact cause cannot be determined. The trigger point can be stress, infection, injury, hypothermia or overheating. A person’s lifestyle, diet, as well as hereditary predisposition - the presence of a certain variant of a gene - are of great importance.

Both T-lymphocytes, which directly kill cells (this happens in type 1 diabetes, multiple sclerosis), and B-lymphocytes, which produce antibodies against their own tissues, which also leads to their death, are responsible for autoimmune damage.

Sometimes antibodies are formed against receptors located on the surface of cells. By binding to the receptor, they can either block or, conversely, activate the cell. This happens, for example, with Graves' disease: autoantibodies block receptors for TSH (thyroid-stimulating hormone), imitating the stimulating effect of the latter, which leads to increased secretion of thyroxine by thyroid cells and the development of thyrotoxicosis.

All autoimmune diseases can be divided into:

• Systemic – affects many organs (examples: systemic lupus erythematosus, rheumatoid arthritis, systemic scleroderma, Sjögren’s syndrome)
• Organ-specific – individual organs and tissues are affected (examples: Hashimoto’s thyroiditis, primary biliary cirrhosis, Crohn’s disease, type 1 diabetes mellitus).

AIZ is characterized by a chronic course with periods of exacerbations and remissions.

Who gets sick more often

Autoimmune diseases affect 5% to 10% of the population. It is considered to be the second leading cause of chronic disease and the third (after heart disease and cancer) cause of disability. AIDS shorten average life expectancy by 15 years.

As already mentioned, the exact cause and the exact triggering factor that triggers AID in a particular patient is very difficult to determine. But there are risk groups that are exposed to these diseases more often than others.

• Women of reproductive age. They suffer from AIDS approximately three times more often than men. And some nosologies, in principle, can only be called female (for example, autoimmune thyroiditis, systemic lupus erythematosus and primary biliary cirrhosis occur in 90% of women).
• Hereditary predisposition. If someone in the family has had this disease, the risk of getting sick increases. In patients with AIZ, a certain set of genes of the HLA system (responsible for the immune response) is detected.
• People who are more susceptible to harmful environmental influences than others. This includes working in hazardous industries, living in an unfavorable ecological zone, chronic and acute intoxication, prolonged exposure to the sun and high temperatures. This also includes smoking and alcohol.
• Bacterial and viral infections. Infectious agents change the structure of antigens and the immune system begins to attack its own tissues. This mechanism has been proven in autoimmune glomerulonephritis after a streptococcal infection, reactive arthritis after gonorrhea, and autoimmune hepatitis after viral hepatitis. More and more scientists are leaning towards the infectious nature of other AIDS.
• Belonging to a certain race. Thus, type 1 diabetes occurs predominantly in whites, while SLE is more common in blacks.
• Traumatic or inflammatory damage to histo-hematological barriers. Normally, some tissues (eye, brain, testes, ovaries) are reliably isolated from the blood, and their antigens are unknown to the immune system. When these barriers are broken, antigens enter the blood and are perceived as foreign. This is how phacogenic uveitis develops after trauma to the lens of the eye, and autoimmune infertility after orchitis.

List of autoimmune diseases

Autoimmune diseases, a list of the most common and the main pathogenesis of their development:

Symptoms of autoimmune diseases

If a person develops a systemic autoimmune disease, symptoms will appear both general throughout the body and specific to specific organs. If we talk about organ-specific AIDs, they start with one organ, but then also affect the entire body. For example, only the pancreas is affected by the autoimmune process in diabetes mellitus. But a lack of insulin as a result of this process leads to the development of chronic hyperglycemia, which affects all organs and tissues.

Diabetes mellitus type 1

Initial symptoms include thirst, weight loss, and increased appetite. The disease can immediately debut with hyperglycemic coma. As it progresses, complications develop: vision deteriorates, kidney failure develops, limbs go numb, and gangrene may develop. Diabetes mellitus accelerates the development of atherosclerosis, hypertension, heart attacks, strokes, and aggravates the course of infectious diseases.

Rheumatoid arthritis

The disease begins with damage to small joints (hands, wrists, ankles). Pain, swelling, and stiffness of movement are noted. Over time, the joints become deformed and complete ankylosis (immobility) may occur. Other organs are also affected - kidneys (amyloidosis), heart (pericarditis, vasculitis), lungs (pleurisy), blood (anemia, neutropenia).

Systemic lupus erythematosus

The disease is characterized by systemic damage. Manifested by fever, weight loss, and a “butterfly” rash on the face. The kidneys, lungs, heart are affected, in the blood - anemia, thrombocytopenia and leukopenia. The nervous system may also be involved - encephalitis, polyneuritis, convulsions.

Systemic scleroderma

In most patients, it is manifested by thickening of the skin, vascular spasms (Raynaud's syndrome), damage to joints and sometimes internal organs.

Graves' disease

With this disease, the level of thyroid hormones is increased, so all the symptoms of thyrotoxicosis are revealed: weight loss against the background of increased appetite, palpitations, shortness of breath, sweating, irritability, exophthalmos (protrusion of the eyeballs). The enlargement of the thyroid gland itself is also noticeable.

Autoimmune thyroiditis (Hashimoto's thyroiditis)

Very rare, but there may be pain, enlargement of the thyroid gland, and discomfort in the neck area. The disease is mainly manifested by hormone deficiency (hypothyroidism). This is weight gain, swelling, weakness, fatigue, drowsiness. Sometimes thyrotoxicosis may be observed at the initial stage.

Multiple sclerosis

The disease can manifest itself with various neurological disorders. Initial signs may be impaired sensitivity in the limbs, unsteady gait, decreased vision, and double vision. The progression of the disease is characterized by muscle weakness, impaired movement, urinary retention, and constipation. In later stages, paralysis of the limbs, urinary and fecal incontinence are noted.

Celiac disease

This pathology is caused by the production of antibodies to gliadin, a component of the gluten protein found in cereals (wheat, rye, barley). When gluten products enter the intestines, massive inflammation and damage to the villi occurs.

As a result, malabsorption syndrome develops - diarrhea, malabsorption, and abdominal enlargement. The disease is genetically determined and manifests itself in children 9-12 months after the introduction of complementary foods. But the latent form may not appear in childhood, but become activated in adulthood.

Sjögren's syndrome

It can be either primary or secondary against the background of other AIZ. The most common symptoms are xerophthalmia (“dry eye”) and xerostomia (“dry mouth”). Other mucous membranes (esophagus, stomach, trachea, genitals) may also be affected.

Ankylosing spondylitis (ankylosing spondylitis)

The process involves the sacroiliac joints, cartilage and bone tissue. Initial manifestations are progressive stiffness in the spine, pain that gets worse at night. Stiffness in the joints, immobility of the spine, and muscle atrophy gradually develop.

Crohn's disease

Characterized by inflammation of the intestinal mucosa. It manifests itself as diarrhea, abdominal pain, fever, anemia, and can be complicated by bleeding and intestinal fistulas.

Nonspecific ulcerative colitis

The colon mucosa is affected - tenesmus, bloody diarrhea, pain, fever . The risk of colon cancer increases 5-7 times.

Myasthenia gravis

The disease most often begins with eye symptoms - drooping eyelids, double vision. Then comes progressive weakness of the muscles of the limbs and difficulty swallowing. Symptoms are not constant and decrease after rest.

Autoimmune hepatitis

For a long time it is asymptomatic or with nonspecific symptoms: weakness, fatigue, joint pain. Jaundice, bleeding, varicose veins are already signs of a late stage, leading to cirrhosis. It is diagnosed by changes in blood tests characteristic of liver inflammation, while viral hepatitis is not detected.

Primary biliary cirrhosis

The first signs may be itchy skin, severe weakness, sleep disturbances, xanthomas (cholesterol plaques) on the skin. Later, jaundice and all the signs of cirrhosis appear: ascites, edema, expansion of the saphenous veins in the abdomen, bleeding .

Dressler syndrome

Autoimmune inflammation, sometimes complicating myocardial infarction. It manifests itself as pericarditis, pleurisy and pneumonitis, developing within 2-6 weeks after a heart attack.

Antiphospholipid syndrome

This state of hypercoagulability can be manifested by arterial and venous thrombosis, habitual miscarriages in pregnant women, thrombocytopenia, anemia, and skin manifestations (a characteristic reticular pattern of the skin).

Pulmonary sarcoidosis

In the acute period, fever, joint pain, erythema nodosum, and severe weakness are possible. As it progresses, shortness of breath, dry cough, and chest discomfort or pain are noted. However, the disease can be asymptomatic and detected only by radiographic examination.

Chronic glomerulonephritis

Characterized by damage to the glomeruli of the kidneys. Clinically, this is manifested by the appearance of blood and protein in the urine, increased pressure, edema, and progression of renal failure.

Vitiligo

A disorder of skin pigmentation, manifested in the appearance of non-pigmented white spots of various sizes and shapes. It only bothers me as a cosmetic defect.

Idiopathic thrombocytopenia (Werlhof's disease)

A decrease in platelets in the blood below 150·10 9 /l in the absence of other causes of this pathology. It manifests itself as bruises, pinpoint hemorrhagic rashes on the skin, and bleeding that does not stop for a long time.

Psoriasis

The most common autoimmune skin disease. It manifests itself in the formation of dry spots raised above the surface of the skin. They can merge with each other, forming plaques that look like frozen spots of wax or paraffin. The disease occurs with periods of remission and exacerbations. Damage to joints and nails is often observed.

Diagnostics of AIDS

Stages of diagnosing autoimmune diseases:

Clinical diagnosis

An autoimmune process is indicated by the chronic course of the disease and resistance to conventional treatment. Some AIDS have common clinical and laboratory signs. Thus, systemic connective tissue diseases (collagenosis) usually result in an increase in blood ESR, as well as an increase in fibrinogen, gamma globulin, and C-reactive protein. Common clinical symptoms may be prolonged fever, weakness, unmotivated fatigue, and weight loss.

Some AIDS have such a typical clinical picture that a diagnosis can be made:

• based on examination (for example, psoriatic plaques, “butterfly” on the face with SLE);
• survey (nature of pain in rheumatoid arthritis, ankylosing spondylitis);
• examination results (hyperglycemia in children or young adults indicates type 1 diabetes mellitus, detection of “cobblestone” changes in the intestinal mucosa indicates Crohn’s disease, etc.)

Immunological tests

Not all AIDS can be diagnosed based on the clinical picture. It is advisable to confirm their autoimmune nature by testing specific autoantibodies.

For some diseases there are mandatory tests that are specific only to these diseases, for example:

• RF (rheumatoid factor) and ACCP (antibodies to cyclic citrullinated peptide) for rheumatoid arthritis.
• Antibodies to TSH receptors in Graves' disease.
• Antibodies to TPO (thyroid peroxidase) in autoimmune thyroiditis.

Other antibodies are nonspecific and are found in different AIDS. Thus, ANF (antinuclear factor), antibodies to native DNA, antiphospholipid antibodies are detected in systemic lupus erythematosus, Sjogren's syndrome, scleroderma, antiphospholipid syndrome. Their detection helps make a diagnosis only in combination with typical symptoms.

There are many other immunological tests, common and not so common, that can confirm AIZ in doubtful cases. You should not try to prescribe a test for yourself; it is better to consult a specialist.

HLA antigen testing

These are histocompatibility antigens, found on the surface of any cell, and they determine the immune response. The set of HLA antigens is unique for each person, and it has been noted that some of them are, to one degree or another, associated with the occurrence of a certain AIZ, so their study is sometimes used for differential diagnosis.

The most commonly used test at present is HLA-B27, which is detected in 90% of patients with ankylosing spondylitis and Reiter's syndrome.

Presumably autoimmune diseases

The list of diseases with autoimmune pathogenesis is constantly growing. It may happen that this list will soon include those diseases that are now considered from other positions.

Of greatest interest is, for example, the hypothesis of the autoimmune nature of atherosclerosis. After all, atherosclerosis of the arteries is the main cause of mortality throughout the world. More and more scientists are arguing that the cause of heart attacks and strokes is not high cholesterol levels, but the degree of inflammation to which the atherosclerotic plaque is exposed. Therefore, risk factors have recently included not only lipid levels, but also the level of C-reactive protein as a marker of chronic inflammation.

Also, such common pathologies as Alzheimer's disease, glaucoma, endometriosis and some others are supposedly classified as AIZ.

Which doctor should I contact?

Unfortunately, there is no dedicated specialist for autoimmune diseases. While this would be a good idea, efforts are already being made abroad to create a separate service for this.

The profile of the doctor who identifies and treats the disease depends on which system or organ is affected.

• Endocrinologist: diabetes mellitus, thyroid diseases.
• Gastroenterologist: Crohn's disease, ulcerative colitis, autoimmune gastritis, autoimmune hepatitis, primary biliary cirrhosis.
• Hematologist – autoimmune anemia and thrombocytopenia.
• Dermatologist – psoriasis, vitiligo, alopecia areata.
• Rheumatologist – systemic lupus erythematosus, rheumatoid arthritis, ankylosing spondylitis, systemic scleroderma, vasculitis, Sjogren's syndrome.
• Neurologist – multiple sclerosis, Guillain-Barré syndrome, myasthenia gravis.
• Gynecologist – autoimmune infertility, antiphospholipid syndrome.

Can AIDS be cured?

Since autoantigens cannot be removed from the body, these diseases cannot be completely cured. They occur with periods of remissions and exacerbations, but the process of self-destruction to one degree or another is constant.

Treatment is aimed at suppressing the immune response and relieving symptoms. There are very rare cases of self-healing of AIDS, but this is as much a mystery to medicine as the reasons for their occurrence.

Autoimmune diseases and vaccinations

Can vaccinations cause AIDS, since they stimulate the immune system? Can patients with AIDS be vaccinated? Such questions arise very often.

These questions cannot be answered unambiguously. Publications from both supporters of vaccination and its opponents constantly appear in the scientific community. Brief conclusions so far are:

• The number of cases of AIDS occurring after vaccination is very small and comparable to chance. Therefore, vaccinations are not considered to be the cause of the development of these diseases.
• Vaccinations prevent the development of infectious diseases, which are largely considered as triggers of autoimmune diseases.
• Most AIDS are associated with increased susceptibility to infections (for example, children with diabetes mellitus). Therefore, refusal to vaccinate poses a greater risk of infectious diseases, which can be severe.

Thus, in any case, vaccination has more benefit than harm. But an individual approach is always needed.

Should I take immunostimulants?

Immunostimulants seem to many to be a universal solution to the problem of frequent colds and recurrent infections. Patients often ask the doctor to prescribe “something to strengthen the immune system.”

Doctors themselves increasingly strongly discourage taking immunostimulants left and right. Immunity is a very complex system; it cannot be determined by conventional tests. And frequent colds are not yet a symptom of immunodeficiency. It is possible to “stimulate” our defense so much that it begins to attack its own body.

In some cases, such drugs are very necessary, but they should be prescribed by an immunologist after a thorough examination. But this is if we are talking about real immunostimulants, which activate that part of the immune system, the deficiency of which is noted based on the analysis.

The same drugs that are advertised in large quantities as strengthening the immune system (so-called interferon inducers), for the most part do not act at all, or only as a placebo. Perhaps this is better.