Autoimmune diseases classification. Autoimmune diseases: causes and mechanisms. Hypotheses for the occurrence of autoimmune diseases

Rice. 19. Activation of T-helper lymphocytes under the influence of superantigen: a - classical activation pathway; 6 - activation by superantigen.

Activation of helper T lymphocytes under the influence of superantigens occurs in a completely different way. In this case, the superantigen is not taken up by the antigen-presenting cell and does not undergo normal digestion (processing) to form a peptide. In this case, the superantigen bypasses this stage necessary for specific recognition and nonspecifically binds to the variable part of the beta chain of the T-cell recognition receptor outside its antigen-specific zone (site). A peculiar cross-linking of the molecules of the major histocompatibility complex of the antigen-presenting cell with the T-cell recognition receptor occurs. In the case of such a mechanism of activation of helper T-lymphocytes, simultaneous activation of a large number of them is possible.
Thus, the distinctive features of stimulation of T lymphocytes under the influence of superantigens are as follows:

1. This does not require digestion (processing) of the antigen in the antigen-presenting cell;
2. Such stimulation does not depend on the antigen specificity of the HLA complex molecules and the T-cell recognition receptor;
3. Superantigen is capable of stimulating 103-104 times more lymphocytes than processed antigen;
4. An allogeneic (foreign) superantigen can stimulate both helper (CD4+) and killer (CD8+) T lymphocytes;
5. Autologous (self) superantigen can stimulate only T-lymphocytes-helpers (CD4);
6. For full stimulation of T-lymphocytes by a foreign superantigen, an additional, costimulatory signal is required.

1. Theory of genetic predisposition. According to modern data, there is a genetically determined predisposition to the development of autoimmune diseases. This predisposition is controlled by at least six genes located on different chromosomes. Some of them are located in the human major histocompatibility complex (HLA), the role of which. in the implementation of the immune response is paramount. It has been established that most autoimmune diseases are associated with the presence of the following antigens in the human HLA phenotype: DR2, DR3, DR4 and DR5. For example, rheumatoid arthritis is associated with HLA-DR4, thyroiditis. Hashimoto's - with HLA-DR5, multiple sclerosis - with HLA-DR2, systemic lupus erythematosus - with HLA-DR3.

1. According to the receptor hypothesis, one of the earliest, certain HLA antigens are receptors for viruses, facilitating their fixation and penetration into the cell. This hypothesis has many arguments both in its favor and against. For example, with such a disease of clearly viral etiology as polio, as well as with infectious mononucleosis, no reliable correlation with HLA antigens is found.

1. Hypothesis about the influence of a hypothetical Ir gene on susceptibility to diseases (impaired selection of antigenic determinants, the presence of “holes” in the repertoire of T-lymphocytes, impaired suppression mediated by T-lymphocytes).

1. Theory of molecular mimicry. The term “mimicry” was once proposed to explain the similarity and identity of the antigenic determinants of some microorganisms to the antigenic determinants of the host, and therefore their recognition by the immune system does not occur, which determines the development of an infectious disease. Currently, the theory of molecular mimicry has changed and is presented in two versions (Fig. 20).

Rice. 20. The role of mimicry in the development of autoimmunity (explanation in the text).

1. generation of cytotoxic T-lymphocytes. In the first defense mechanism, antibodies attack extracellular infectious agents and their toxins, forming immune complexes; with the second mechanism, in order to save the entire organism, cytotoxic T-lymphocytes have to destroy their own cells in which intracellular pathogens are hidden.

1. The presence of autoantibodies or cytotoxic T lymphocytes directed against the antigen associated with the disease.
2. Identification of the autoantigen against which the immune response is directed.
3. Transfer of an autoimmune process using serum containing antibodies or cytotoxic T lymphocytes.
4. The possibility of creating, by introducing an autoantigen, an experimental model of the disease with the development of corresponding morphological abnormalities characteristic of the disease.

1. The presence of specific autoantibodies;
2. The presence of specific cellular sensitization (detected using the blast transformation reaction - RBT and the leukocyte migration inhibition test in the presence of the corresponding autoantigen);
3. Increased levels of gamma globulin and/or IgG;
4. Changes in the number of T-helpers and T-suppressors, leading to an increase in the immunoregulatory index;
5. Decrease in the level of C3 and C4 complement components;
6. Deposits of immune complexes in affected tissues (IgG, IgM, C3, C4 and fibrin);
7. Lymphoid cell infiltration of affected tissues;
8. Determination of HLA phenotype.

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.

Description of the presentation Autoimmune diseases and mechanisms of their development Autoimmune on slides

Autoimmune diseases are diseases in the pathogenesis of which immune mechanisms directed against one’s own tissues (auto. Ag) are involved. The central mechanism of autoimmune diseases is a defect in immunological tolerance, leading to the activation and expansion of auto. Ag-specific T- and B-clones and, as a consequence, the production of circulating auto. At and countless cytokines and other inflammatory mediators.

Immunological tolerance (unresponsiveness) (Latin tolerantia - tolerance, tolerance) is the body’s inability to mount an immune response to a specific antigen while maintaining immunological reactivity to other antigens. May be temporary. ! That is, in addition to a specific immune response, the body is capable of developing specific unresponsiveness to the antigen. Immunological tolerance is specific.

The phenomenon of specific unresponsiveness is a physiologically normal process that manifests itself in ontogenesis and is aimed at creating unresponsiveness to one’s own tissues. Violation of this process leads to autoimmune lesions - immunological reactions to the body's own (auto-) antigens. Conventionally, they distinguish: - tolerance to one’s own - self-tolerance - artificially induced tolerance to something foreign - non-self tolerance

Self-tolerance During normal physiological processes, clonal depletion of autoreactive clones in the thymus, bone marrow and the state of anergy in the periphery exclude T and B cells from their work, which are capable of recognizing their own Ags.

Tolerance to “one’s own” (self-tolerance) is formed in 2 ways: Central tolerance T l autoapoptosis - Negative selection (clonal deletion, clonal depletion) in the thymus (T lymphocytes) and bone marrow (B lymphocytes)

Figure 13 -9 AIRE expression ((autoimmune regulator) determines the immune repertoire in the thymus AIRE is a transcription factor expressed in the medullary/medullary layer of the thymus

Tolerance to “one’s own” (self-tolerance) is formed in 2 ways: T l. Central tolerance Peripheral tolerance T l autoapoptosis - Negative selection (clonal deletion, clonal depletion) in the thymus (T lymphocytes) and bone marrow (B lymphocytes) - Inactivation of own clones in the periphery (either 1 due to lack of co-stimulation by T lymphocytes or Mf, or 2 due to too low level of expression of the complex of its own peptides with MHC class I and II molecules). CD 28 anergy apoptosis no costimulation

The presence of pathogenetic changes and violation of autotolerance lead to the activation of “forbidden” clones and the development of autoimmune diseases

Autoimmune diseases (AIDs) A group of more than 100 nosological forms and conditions in which the characteristics of the immune system lead to specific immune reactions against one’s own antigens (Shoenfeld Y., 2008). AIDs affect 5-7% of the world’s population, developing more often in women than in men (9:1), as a rule, at a young age, AIZ is considered the most common chronic human pathology 103 sets of diagnostic criteria, constantly supplemented and revised

Prevalence of autoimmune diseases Incidence of AIZ Diseases Population frequency Frequent Autoimmune thyroiditis, rheumatoid arthritis, psoriasis 0.1 -1% Rare Systemic lupus erythematosus, type 1 diabetes, Multiple sclerosis, celiac disease, vitiligo 0.01 -0.0001% Very rare B. Addison , Goodpasture sm, Guillain-Barre sm Less than 0.0001% Shoenfeld Y. et al. Diagnostic Criteria of Autoimmune Diseases —

“Autoimmunity” - the ability of immune system cells to recognize antigenic determinants of their own tissues - a normal component of the physiological immune response - MHC class I and II molecules - Idiotypic Ig determinants - Idiotypic TCR determinants

AIZ includes pathological conditions in which dysregulation of physiological autoimmune processes leads to the development of cellular and humoral immune reactions against components of one’s own tissues, causing structural and/or functional disorders in target organs

Organ-specific - react with peptide hormones (insulin), cellular receptors for hormones and neurotransmitters (TSH, AChR, etc.) or proteins specific to certain organs (thyroglobulin); Cell-specific – directed against the protein components of biological membranes of various cells (er, tr, lf); Organ-nonspecific - react with molecules widely distributed in various cells that participate in cellular activation and metabolism (NA, NP, cytoskeletal proteins, cytoplasmic enzymes, etc.), blood plasma proteins (Ig, C, coagulation cascade proteins), etc. .

Auto disease. Ag Immune response Organ-specific diseases Addison's disease adrenal glands auto. At AIGA membrane antigens Er auto. At Goodpasture's syndrome basement membrane of the kidneys and lungs auto. At Graves' disease TSHR auto. At (stimulating) Thyroiditis Hashimoto TPO, TG cell-mediated cytotoxicity, auto. At AITP membrane antigens Tr auto. At type 1 diabetes β-cells of pancreatic islets cell-mediated cytotoxicity, auto. At Myasthenia Gravis AHR auto. At (blocking) Poststreptococcal glomerulonephritis of the kidney CEC Infertility sperm, testicles auto. At Multiple sclerosis myelin Th1 and CD 8+ cells, auto. At Systemic diseases Rheumatoid arthritis connective tissue, Ig. G auto. At, CEC Scleroderma heart, lungs, gastrointestinal tract, kidneys, auto cell nuclei. At Sjögren's syndrome salivary glands, liver, kidneys, thyroid auto. At Systemic lupus erythematosus (SLE) DNA, nuclear proteins, membrane antigens Er and Tr auto. At, CEC Classification of autoimmune diseases

Pathogenesis is a violation of the tolerance of the immune system to its own organs and tissues, the development of which is mediated by a complex interaction: - Immunogenetic (predisposing) factors, - Immunological factors, - Infectious factors, - Defects in neuroendocrine and hormonal regulation.

Association of MHC class II with AIZ The existence of allelic forms of the HLA system has a pronounced impact on the nature of the immune response. Differences in the amino acid sequence of Ag molecules of the HLA system can provide selective binding of processed antigenic fragments. This process is called determinant selection.

In addition, antigens of the HLA system influence the TCR repertoire during the maturation of the immune system, since they take part in the selection of T-cell clones expressing a specific TCR. This process determines the formation of tolerance to self-tissue antigens and, under certain conditions, the direction of the immune response to self-antigens of the HLA system.

genes mechanism of immunogenetic predisposition HLA system selectively bind to peptides a. AG; expansion of autoreactive T cells; deletion of T cells that control infection of genes encoding TCR synthesis of the number of autoreactive T cells; ↓ ability to control the infection that induces AIZ genes encoding Ig synthesis impairment of AAG presentation, anergy defect, impairment of the AAT synthesis process genes encoding the synthesis of complement components impairment of IR clearance genes encoding the synthesis of sex hormones immune effects of sex hormones encoding the synthesis of cytokines immune effects of cytokines. The role of genes in the predisposition and development of AISAID

Etiological factors for the development of AIZ (pathogenesis): - release of anatomically hidden antigens (MBP, TPO, Ag of the anterior chamber of the eye and testicles) - loss of self-tolerance to antigens of barrier tissues; — molecular mimicry is a popular theory. Some viruses and bacteria have antigenic determinants that are similar to human antigens. Most AIDS are associated with an infectious disease or a specific pathogen (type 1 diabetes and Coxsackievirus, ankylosing spondylitis with Klebsiella, hsp 65 and RA, etc.);

Molecular mimicry between proteins of infectious pathogens and human antigens Protein Residue † Sequence ‡ Human cytomegalovirus IE 2 79 P D P L G R P D E D HLA-DR molecule 60 V T E L G R P D A E Poliovirus VP 2 70 S T T K E S R G T T Acetylcholine receptor 176 T V I K E S R G T K Pap illoma virus E 2 76 S L H L E S L K D S Insulin receptor 66 V Y G L E S L K D L Rabies virus glycoprotein 147 T K E S L V I I S Insulin receptor 764 N K E S L V I S E Klebsiella pneumoniae nitrogenase 186 S R Q T D R E D E HLA-B 27 molecule 70 K A Q T D R E D L Adenovirus 12 E 1 B 384 L R R G M F R P S Q C N Gliadin 206 L G Q G S F R P S Q Q N Human immunodeficiency virus p 24 160 G V E T T T P S Human Ig. G constant region 466 G V E T T T P S Measles virus P 3 13 L E C I R A L K Corticotropin 18 L E C I R A C K ​​Measles virus P 3 31 E I S D N L G Q E Myelin basic protein 61 E I S F K L G Q

Cross-reacting hypertension non-professional. APCinduction of MHC– Th 2 Th 1 IL-4, IL-10 inf, IL-2 T TAPC APC* AIZ Pathways for activation of immunologically ignored T lymphocytes 1. Changes in endosomal enzymes lead to the expression of hidden (cryptic) epitopes during processing. 2. Involvement of non-professional phagocytes and expression of MHC II on them.

Etiological factors for the development of AIZ (pathogenesis): - release of anatomically hidden antigens (MBP, TPO, Ag of the anterior chamber of the eye and testicles) - loss of self-tolerance to antigens of barrier tissues; - “with ryptic - self” hypothesis (based on the fact that self-antigens are presented in the thymus in a complex with MHC molecules and are subject to negative selection); - local overproduction of IFN-γ or trauma can induce an immune response against hidden autoantigens (aberrant expression of MHC class II); — molecular mimicry is a popular theory. Some viruses and bacteria have antigenic determinants that are similar to human antigens. Most AIDS are associated with an infectious disease or a specific pathogen (type 1 diabetes and Coxsackie virus, ankylosing spondylitis with Klebsiella, hsp 65 and RA, etc.); — hormonal background (predisposing factor); - defective apoptosis (appearance of auto. Ab to bcl-2, c-myc-, p 53; mutations Fas. R and Fas. L); — imbalance in Th1/Th2 production; - neuroendocrine disorders; — dysfunction of the immune system (impaired elimination/apoptosis of autoreactive clones in the central organs of immunogenesis)

Tn 1 Tn 2 IL-2 inf-IL-4, IL-5, IL-13, IL-10 RA diabetes mellitus allergic diseases HIV infection inhibition autoimmune thyroiditis systemic lupus erythematosus systemic scleroderma. Immunoregulatory disorders in AIZ

1 Polyclonal activation. Mechanism of induction of an autoimmune response 2 IFN-γ Tissue damage and development of AIZ 3 4 5 Development of local inflammation Production of auto. At. Target cell/organ

Allergic reactions of the 2nd type (2nd type of hypersensitivity) Humoral cytotoxic immune reactions, which are based on the formation of Abs to primary or secondary structures of the cell surface.

Disease/Syndrome Auto. Ag Effect AIHA (autoimmune hemolytic anemia) Rh, group Ag of erythrocytes destruction of Er (C and Fc. R phagocytes) AITP (autoimmune thrombocytopenic purpura) Gp IIb; IIIa platelet bleeding Goodpasture's syndrome Collagen type IV BMP glomerulonephritis, lung damage Pemphigus vulgaris Epidermal cadherin skin lesions (blisters) Acute rheumatic fever Ag Str. , cross-reacting with cardiomyocytes Arthritis, myocarditis. Classification of AIZ depending on the type of immune response and mechanisms of tissue damage (type 2 hypersensitivity)

Allergic reactions of the 3rd type (IC pathology) Pathogenesis CIC initiates its pathogenic effect through activation of plasma components and activation/inactivation of blood cells

Disease/Syndrome Auto. Ag Effect Systemic lupus erythematosus (SLE) DNA, histones, ribosomes, RNA Glomerulonephritis, vasculitis Rheumatoid arthritis (RA) RF (At-Ig. G) Glomerulonephritis, vasculitis. Classification of AIZ depending on the type of immune response and mechanisms of tissue damage (type 3 hypersensitivity) Characterized by massive lymphomacrophage infiltration and pronounced cellular cytolysis

Allergic reactions of the 4th type (T-cell-mediated cytotoxicity) With this type of pathology, specific sensitized T lymphocytes and Ag in dissolved or granular form enter into a reaction. The result is the implementation of the cytotoxic effects of Mf and T cells.

Disease/Syndrome Auto. Ag Effect Insulin dependent diabetes mellitus (type 1 diabetes) β -cells of pancreatic islets Destruction of β -cells Multiple sclerosis Myelin basic protein paralysis. Classification of AIZ depending on the type of immune response and mechanisms of tissue damage (type 4 hypersensitivity)

Disease/Syndrome Auto. Ag Effect Graves' disease TSHR thyrotoxicosis Myasthenia Gravis AChR Impaired contraction of striated muscles. Classification of AIZ depending on the type of immune response and mechanisms of tissue damage (type 5 hypersensitivity)

Diagnostic criteria for autoimmune diseases Level of evidence Explanations Level 1: Direct evidence 1. Transfer of the disease with the introduction of autoreactive serum - from person to person, - in the experiment AITP is a classic example, - transplacentally thyrotoxicosis, myasthenia gravis 2. Detection of auto. AT AIHA 3. Disease transfer with the introduction of autoreactive lymphocytes DM type 1 level 2: Indirect evidence 1. Possibility of creating an experimental model of AIZ - spontaneous (genetically determined) NOD, NZB line of mice - experimentally induced EAE, thyroiditis, AI orchitis (immunization ) - neonatal thymectomy evidence of peripheral tolerance - genetic manipulation, knock - outs level 3: Additional evidence 1. T-cell reactivity to auto. Ag in vitro 2. Gender 3. Histopathology 4. Presence of chronic infection 5. Good response to immunosuppressive therapy 6. Association with MHC (HLA)

Therapy for AIZ: - Immunosuppression (glucocorticosteroids, cyclophosphamide, azathioprine, cyclosporine A) - Plasmapheresis - Thymectomy

Specific therapy for AIZ - T-cell vaccination - MAT - blockade of MHC peptides - induction of “oral tolerance” - anti-cytokine therapy (anti-TNF-α in RA) - anti-inflammatory cytokine therapy (IFN-β in MS) - gene therapy

Autoimmune endocrinopathies are autoimmune diseases of the endocrine system in which auto. Ab or autoreactive T-lymphocytes reacting with Ag of the endocrine glands

As an auto. Ags in these diseases are: tissue-specific membrane receptors enzymes secreted hormones

Disease Organ/target cell Auto. Ag Diabetes mellitus type 1 (type 1 diabetes mellitus, IDDM) Autoimmune thyroiditis Addison's disease Chronic active hepatitis Autoimmune parathyroidism Hypogonadism B-cells of the pancreatic islets Thyroid epithelium Adrenal cortex Hepatocytes Parathyroid glands Testes, ovaries GAD-65, 67 ICA-512 TPO , TSHR, Tg, T 3, T 4, TSH 21 -OH (21 -hydroxydase) LKM-1 Ca 2+ - p450 receptor - cytochrome 17 - α -hydroxylase. The most common autoimmune diseases of the endocrine system

Type 1 diabetes is a complex multifactorial autoimmune disease of genetic nature, in which long-term chronic lymphocytic insulitis leads to the destruction of pancreatic β-cells with the subsequent development of insulin deficiency. In Eastern European countries, type 1 diabetes ranks second among chronic diseases in children.

Phases of destruction of β -cells of the islets of Langenhars in type 1 diabetes Age (years) Number of β -cells per Genetic. Immunol. Progressive Clinic Clear predisposition. disorders decrease diabetes insulin N insulin level N glucose glucose

Genetic predisposition - the risk of developing type 1 diabetes in Caucasians is 0.4% - in children born from sick mothers, the risk increases to 3%; from sick fathers – 9%; if both parents are sick - 30% - Association with HLA-DR 3/DR 4 (95% of patients)

In diabetes mellitus, functional disorders of the cellular component of immunity occur long before the manifestation of the disease and are caused by a breakdown in tolerance to islet antigens. Auto identification. Ag is important because: 1. Autos detected for them. Abs are serological markers of the disease; 2. Modulation of the immune response to auto. Ag is the basis of pathogenetic specific treatment of diabetes

Characteristics of auto. Ag in type 1 diabetes 1. GAD – 65, 67. Mm 64 k. Yes, catalyzes the conversion of glutamic acid into γ-aminobutyric acid. Automatic antibodies are detected in 90% of cases. 1. IA -2 α and IA 2 β (protein tyrosine phosphatase), transmembrane proteins belonging to the tyrosine phosphatase family. Auto. Abs are detected in 65% of cases. 2. ICA-512 (islet cell antigen) 3. Insulin is the only organ-specific Ag 4. Insulin receptor 5. Carboxypeptidase

The role of environmental factors: The implementation of genetic predisposition to type 1 diabetes significantly depends on the action of certain environmental factors: Viruses: A) act cytotoxically on β-cells B) viral Ags are presented on the surface of β-cells with the subsequent development of autoimmune reactions C ) viruses can induce the generation of specific effector T lymphocytes that cross-react with β-cell antigens: - vir. Coxsackie B – cross-reacts with GAD, – vir. Rubella - cross-reacts with insulin, - retroviruses - retroviral proteins are super. Ags that stimulate the generation of autoreactive T cells

— Nutrition factors – animal proteins, sugars, nitrates/nitrites. It is believed that a functional overstrain of β-cells occurs, as a result of which the expression of Ag on these cells increases. — Sex hormones — Stress

apoptosis autoreactive TLF-cell Fas. Mechanisms of damage to β-cells: 1. The leading role is the cytotoxic activity of CD 8 + Lf-s, directed against β-cell Ag, presented to Th-cells in combination with MHC class I. There are 2 independent pathways of T-cell cytotoxicity - Exocytosis of perforin-containing granules on target cells (perforin induces lysis); — Through Fas + Fas. L: Normally, pancreatic cells do not express Fas, however, during the development of insulitis, various cytokines and inflammatory mediators (IL-1; NO) up-regulate expression. The result of this is cellular destruction due to Fas-induced apoptosis. Selective expression of Fas on -cells and the absence of Fas on - and -cells during the process of insulitis explains the selective damage to the cells of the pancreatic islets 3. O 2 radicals 4. ADCC (via Fc to NK, Mn/Mf, TLf)

Prediabetes type 1 diabetes. Free radical processes. AI processes without clinical manifestations and autoimmunity is humoral - cellular Environmental factor (viruses, cow's milk) Genetic factor (HLA, gene - TCR chains, insulin gene, NOs gene) DNA cells O 2 - NAD (ADP-ribose) npoly-ADP -ribose synthetase (PARS) insulin deficiency o Immunomodulation (T-activin, nonspecific stimulation) Antioxidant therapy (aminoguan o zine, nicotinamide) Insulin therapy o drugs that prevent further progression (T-activin, antioxidants) Breastfeeding o Vaccinations against enteroviruses o Vaccination (genetic therapy) o Avoid trigger factors Treatment and prevention of type 1 diabetes

Type 3 immunopathology The term “IR disease” refers to a group of diseases resulting from the deposition of IR in various organs and tissues, including the glomeruli of the kidneys and the walls of blood vessels.

Systemic lupus erythematosus (SLE) is a systemic autoimmune IR disease characterized by diverse clinical manifestations and disorders of cellular and humoral immunity, leading to hyperproduction of auto. AT and accompanied by deposition in the tissues and cells of the body of pathogenic auto. AT and IR. The pathological process involves connective tissue, vessels are affected, vasculitis, thrombosis, arthritis, nephritis, neurological disorders, etc. develop. Women of reproductive age are affected in 90%.

Characteristics of auto. AT auto AT frequency of occurrence, % auto. AG antinuclear antibodies (=ANF) 1 95 multiple nuclear and cytoplasmic AGs anti-ds. DNA 2 60 -83 native double-stranded DNA anti- s s. DNA 60 -70 native single-stranded DNA anti-Sm AT 3 30 -40 polypeptide, part of nuclear RNA anti-Ro (ss. A) 4 30 -40 RNA polymerase AT to nucleosome 5 30 nucleosome, type IV collagen anticardiolipin 50 phospholipid anti-erythrocyte AT 60 AG surface of erythrocytes antilymphocyte 70 AG surface of leukocytes AT to cytoplasmic components 50 AG mitochondria, ribosomes, lysosomes RF 30 Ig. G

Etiology and pathogenesis 1. Genetic predisposition to the disease in 10% of patients - close relatives also become ill; in 50-70% of identical twins the disease occurs (concordance) association with HLA: HLA - DR 2 (associated with deficiency of C 2 and C 4 .) HLA - DR 3 (associated with anti. Ro (ss. A) AT) HLA - A 1, B 8, B 15 - 33% in 20% of patients hereditary deficiency of C 2 and C 4 complement components hereditary or acquired defect CR 1 Fc γRIIa polymorphism affects the metabolism of IR, thereby affecting the clinical course of SLE.

2. The effect of viruses on the body: due to lymphotropy - a direct effect on IS and disruption of the immunoregulation mechanism; viral infection through the process of cellular destruction leads to the release of endogenous DNA, which directly stimulates autoimmunization; viruses containing DNA can cause the production of antibodies to DNA; polyclonal B-cell activation (EBV) reaction to modified lymphocytic Ags due to viral infection Antibodies are detected against DNA and RNA containing viruses: VEB, CMV (herpes virus family) Mixo- and paramyxoviruses (found in skin and kidney biopsies, as well as LF of SLE patients ) Retroviruses (46% of patients with SLE have antibodies to HIV proteins, as well as to oncoviruses, human T-cell leukemia virus)

3. Hormonal and reproductive factors (impaired estrogen metabolism) 4. Disruption of immunoregulation processes 5. The role of ultraviolet radiation and free radical reactions in the body According to the FREE RADICAL THEORY of the pathogenesis of SLE, the initial hereditary defect in SLE leads to an increase in the formation of auto. AG from nuclear components due to free radical reaction (FRR) In support of the hypothesis, a connection between the onset of the disease and exacerbation of SLE with factors that increase endogenous FRR is revealed: In people with impaired clearance of apoptotic cells, ultraviolet irradiation (sun) induces FRR, damaging the components of the nucleus and causing other cellular damage to SLE It is more common in women of reproductive age, whose serum copper levels (a known catalyst for CPP) are higher than in men. Oral contraceptives increase serum copper levels and may cause the appearance of LE cells and exacerbation of SLE. In patients with SLE, inhibition of antioxidant defense is observed. It is not known what is primary: increased production of ROS, or a genetically determined decrease in antioxidant protection. Viruses, by damaging cells, can also stimulate the formation of ROS.

Nosology Immunofluorescence technique ELISA, counter-electrophoresis, immunoblot CTD: SLE, RA, JRA, SSc, dermatomyositis, Sjögren's disease Positive (high titers) AG: ds-DNA, RNP, Sm, Ro, histone (H 1, H 2 A-H 2 B, H 3, H 4), La, Scl-70, Jo-1 DM/Scl, Mi 2, aminoacyl. RNA synthase, DNA polymerase 1, nucleosomes Diseases associated with ANF 1: drug-induced lupus, subacute cutaneous lupus erythematosus, hepatitis, cholangiopathy, Raynaud's syndrome, chronic active hepatitis, thyroiditis, urticaria, post-streptococcal arthritis, undifferentiated connective tissue diseases Positive ( high and low titers) AGs: histone, vimentin, actin, nucleolar, Ro, Scl-70, centromeric, topoisomerase 1, cross with streptococcus Lymphogranulomatosis, lymphoma, sacoidosis Low titers Not determined. Antinuclear antibodies and detection methods (Speransky A. I., Ivanova S. M., 2002)

a anti-DNA- VLf PKDNA+ histone Th cytokine eptide (histone, DNA, nucleosomes) MHC II TCR anti. DNA AT (antihistones, antinucleosomal AT)Mechanism of induction of anti. DNA AT

AIT DM type 1 AIH ulcerative colitis myasthenia gravis AI skin MS SLE SSD DM SV organ-specific AI Th 2 Th 1 organ-nonspecific AI estrogens low doses of CS

Stages of development of autoimmune diseases 1 - Initiation and. O. 2 - Development and. O. on auto. Ag 3 - Development of the disease

It has been established that autoimmunization of the body can result from:

• 1) Release of sequestered antigens into the bloodstream. It is known that these antigens do not participate in the mechanism of negative selection of T- and B-lymphocytes in the thymus and bone marrow, and tolerance does not develop to them among these cells. The interaction of immunocompetent cells with such antigens always leads to the induction of an immune response followed by an immune reaction to these antigens. Examples of sequestered antigens are: myelin basic protein, normally separated from the immune system by the blood-brain barrier, sperm antigens and eye lens antigens. It has been established that during injuries, inflammatory diseases, viral and bacterial infections, these antigens enter the bloodstream;
• 2) The appearance of new antigenic determinants on cells and tissues. This may be the result of a metabolic disorder in tissues and cells (a defect in the synthesis of macromolecules, a violation of their hydrolysis in lysosomes, abnormal protein glycosylation, etc.), modification of cell membranes under the influence of medicinal and toxic substances, a viral infection, or the formation of a single antigenic determinant by an autoantigen with a viral peptide or a medicine. Antibodies that appear during the immunization process, due to their ability to cross-react, are capable of attacking normal tissue and inducing inflammatory-destructive processes in it;
• 3) Molecular mimicry. It has been established that a number of viruses and bacteria contain antigenic determinants identical or similar to human ones. A study of about 600 virus-specific sera capable of reacting with 11 types of viruses showed that in 3% of cases they react with high activity with normal human tissues. These data support the view that molecular mimicry is quite common and common.

The data presented in Table 11-2 indicate that molecular mimicry exists between a wide variety of infectious agents and structures of the human body. In this regard, it should be remembered that the antigenic determinants of proteins (i.e., those formations that induce immune reactions and with which the products of the immune response interact) are often represented by several (7-10) amino acid residues.

The role of molecular mimicry in the development of autoimmune pathology is well demonstrated by the following data: the development of autoimmune encephalitis after immunization of rabbits with the hepatitis B virus polymerase peptide, which is 60% homologous to the human myelin basic protein peptide; the development of myocarditis during streptococcal infection, when antistreptococcal antibodies reveal high reactivity to cardiac muscle antigens, etc. These observations indicate that protective antibodies (cells) produced in response to infection, due to the ability to cross-react with similar structures, can induce autoimmune tissue damage .

4) Increased and atypical expression of HLA molecules on cells. An immunological study of insulin-dependent DIABETES MELLITUS showed that in individuals with this pathology, pancreatic beta cells express class I HLA antigens at a high density, significantly greater than in healthy individuals, as well as class II HLA antigens in large quantities, which cells are not normally expressed at all. Similar data were obtained in the study of Graves' disease. In patients, atypical expression of class II HLA antigens is observed on the glandular cells of the thyroid gland.

It is believed that atypical expression of HLA class II antigens on beta cells of the pancreas and glandular cells of the thyroid gland and their abnormal presentation of antigen are a trigger for autoimmunization of the body. This opinion also has convincing experimental confirmation. Using transgenic mice, it was shown that induction of expression of MHC class 2 molecules on pancreatic beta cells leads to the development of diabetes, which is accompanied by a pattern of lymphocytic infiltration of the islets of Langerhans. Increased, atypical expression of class II HLA antigens on cells that do not normally express it can be induced by substances of both microbial origin and endogenous origin.

In vitro experiments have shown that under the influence of INF-gamma, the expression of class II HLA antigens occurs on various types of cells: intestinal epithelial cells, beta cells of the pancreas, glandular cells of the thyroid gland, hepatocytes, kidney cells. It is noteworthy that in patients with systemic lupus erythematosus during the active course of the disease, an increased level of INF-gamma is observed in the serum. It is known that infections, inflammation, and injuries can act as inducers of this cytokine. An important property of INF-gamma is its ability to induce the production of a number of cytokines, including IL-1. In the development of autoimmune reactions, as follows from a number of studies, this interleukin can act as a costimulator of the activation of clones of autoreactive T lymphocytes.

5) Polyclonal activation of B lymphocytes.

It is known that polyclonal B-cell activation can lead to the production of antibodies of different specificities. When clones of autoreactive B lymphocytes are activated by this mechanism, the resulting autoantibodies are believed to be capable of acting as a trigger for the disease. Many viruses (cytomegalovirus, Epstein-Barr virus, measles virus), bacteria (gram-negative) and their components (toxins, DNA, proteolytic enzymes) have the properties of polyclonal activators. In this regard, it should be noted that systemic autoimmune diseases are always accompanied by the production of autoantibodies of very different specificity: antinuclear, anti-DNA, antibodies to collagen, elastin, T- and B-lymphocytes, platelets, erythrocytes, etc.

It is important to emphasize that the clinical and experimental material accumulated to date indicates the multifactorial etiology of autoimmune diseases. It should also be added that according to modern data, there is a genetic determinacy of their development. It has been established that predisposition to autoimmunopathology is controlled by several genes, some of which are located in the major histocompatibility complex. It has been proven that most autoimmune diseases are associated with the presence of the following antigens in the HLA phenotype: DR2, DR3, DR4, DR5. Rheumatoid arthritis is associated with HLA-DR4, Hashimoto's thyroiditis - with HLA-DR5, multiple sclerosis - with HLA-DR2, systemic lupus erythematosus - with HLA-DR3. Autoimmune diseases develop much more often in women than in men.

Clinical and experimental data indicate that the development of autoimmune diseases is based on the same mechanisms that the immune system uses to protect the body from exogenous intervention - antibodies, cytotoxic T-lymphocytes. The experiment established that helper T-lymphocytes (CD4+ cells) play a leading role in the formation of autoimmune processes. Using a model of experimental autoimmune encephalitis, thyroiditis and arthritis, it was established that these diseases can be transferred from sick animals to healthy animals using sensitized T-helper cells, and also suppressed by administering anti-CD4+ antibodies to animals, which eliminate or suppress the activity of helper T-lymphocytes. The results obtained from the study of experimental encephalitis indicate that the quantitative ratio of Th1 and Th2 cells plays a significant role in the development of autoimmune diseases: Th1 cells contribute to the development of the process, and Th2 cells, on the contrary, block it.

The main pathways for the development of autoimmune reactions are shown in Figure 11-4. In the event of the development of a cellular immune reaction, effector autoreactive T-killers are formed from naïve T-cytotoxic cells with the help of Tn cells. Sensitization of naïve T-cytotoxic lymphocytes occurs when they interact with a self-antigen presented either by the target cells themselves or by antigen-presenting cells in complex with MHC class I molecules. Formed killer T-cells, when they encounter cells carrying this autoantigen (target cells), interact with them using a specific receptor and, through the production of perforins, cause their lysis. Target cell death can also be induced by fragmentins and Fas ligand. In this case, cell death develops through apoptosis. This mechanism of development of autoimmune pathology is characteristic of insulin-dependent DIABETES MELLITUS and multiple multiple sclerosis.

In the event of the development of a humoral immune reaction to a self-antigen, plasma cells are formed from B lymphocytes, with or without the help of T lymphocytes. The autoantibodies they produce can have the following effects:

• 1) lyse cells carrying a specific autoantigen (with the involvement of the complement system in the process). (This mechanism underlies the development of autoimmune hemolytic anemia, Goodpasture syndrome and other diseases);
• 2) have a stimulating effect when interacting with the corresponding antigenic structure. (This result is observed in Graves' disease. Produced autoantibodies to the thyroid-stimulating receptor of thyroid cells, interacting with it, cause unregulated hyperactivation of the thyroid gland, which leads to the development of thyrotoxicosis);
• 3) have a blocking effect. (This effect underlies myasthenia gravis. The autoantibodies produced during this disease suppress the functioning of acetylcholine receptors at neuromuscular synapses and also cause their degradation, which is the cause of the development of the disease);
• 4) form immune complexes by interacting with soluble antigens. (The toxic effect of immune complexes underlies the development of diseases such as post-streptococcal glomerulonephritis, ankylosing spondylitis, rheumatoid arthritis, systemic lupus erythematosus). The tissue-damaging effect of immune complexes lies in their ability to activate the complement system, concentrate granulocytes and monocytes at the site of their deposition, and also activate these cells. Activation of granulocytes and monocytes leads to the production of proteolytic enzymes and polycationic proteins into the surrounding tissues, which, together with activated complement components (MAC, C3a, C5a), cause inflammatory-dystrophic processes in tissues.

The immune system is a complex mechanism consisting of cells and organs. Its main task is to protect humans from the influence of foreign agents. Perfectly distinguishing “strangers” from “friends,” it protects the body from many different pathologies. But sometimes it fails. The immune system loses the ability to distinguish between its cells. The body begins to produce antibodies that attack healthy tissue. In this case, doctors conclude: disturbed autoimmune processes are occurring. What does this mean? And how to deal with such phenomena?

Autoimmune processes in the body - what is it?

Most people who hear about such phenomena immediately associate them with severe incurable diseases. This is true. But only if the autoimmune processes are disrupted. If they are normal, then they perform very necessary and important functions.

Let's figure out what an autoimmune process means. During human life, any disturbances may occur in cells. In this case, they become foreign and can even cause harm. This is where the immune system comes into play. It cleanses the body and rids it of foreign agents. The immune system eliminates dead cells. It is difficult to even imagine what would happen to the body if such a function did not exist. A person would turn into a real cemetery of dead cells. It is this function that is called the “autoimmune process in the body.”

In case of failure, the immune system begins to attack its own cells. It perceives healthy tissues as foreign elements. As a result, their own immune system damages them. Against the background of this phenomenon,

Reasons for violations

Until today, doctors are not ready to say why autoimmune processes are disrupted. The reasons for such phenomena are not fully understood. There is an opinion that such pathologies can be triggered by injuries, stress, hypothermia, and various infections.

Doctors identify the following sources that trigger such disorders in the body:

1. Various infectious pathologies provoked by microorganisms whose protein structure is very similar to human tissues and organs. For example, very often the source of the problem is streptococcus. This infection invades a cell, disrupts its functioning and infects neighboring ones. The protein resembles healthy tissue cells. The immune system is unable to distinguish between them. As a result, a person may develop ailments such as arthritis, autoimmune glomerulonephritis, and gonorrhea.
2. In the body, as a result of a number of reasons, pathological disorders such as necrosis or tissue destruction can be observed. The immune system, trying to cope with them, begins to attack not only the affected cells, but also healthy tissues. For example, hepatitis B often becomes chronic.
3. Rupture of blood vessels. Many organs do not come into contact with this liquid. After all, blood does not fill the entire cavity of the body, but flows through special vessels. But sometimes veins can rupture. In this case, bleeding will begin. The body will immediately react to this phenomenon, perceiving the cells as foreign, and will launch the production of antibodies. Such disorders can lead to thyroiditis and autoimmune prostatitis.
4. The source of the problem may be an immunological imbalance or a hyperimmune state.

At-risk groups

The autoimmune process in the body can be disrupted in any person. However, doctors identify certain groups of people who are most susceptible to this pathology.

1. Women of childbearing age. It has been noticed that young ladies suffer from these disorders much more often than men. In this case, the pathology often develops during reproductive age.
2. People with similar illnesses in their family. Some autoimmune pathologies are genetic in nature. Such a disease is Hereditary predisposition, especially in combination with other factors, often becomes a trigger for the development of pathology.
3. Individuals who have a lot of contact with certain components of the environment. Some substances can become a source of disease development or aggravate existing ones. Such provoking factors are: bacterial, viral infections; chemicals; active sun.
4. People of a certain ethnicity. Doctors state that mainly white people develop a pathology such as type 1 diabetes. in severe stages, most often affects Spaniards and African Americans.

General symptoms

Each case of this disease is quite unique. The symptoms that occur in a person depend on which tissues are attacked. However, there are common marker symptoms that indicate a disturbed autoimmune process.

Signs characterizing a malfunction in the body:

1. The patient experiences dizziness, general weakness, and low-grade fever.
2. Most autoimmune pathologies occur in a chronic form. Stages of remission alternate with exacerbations. Sometimes the pathology progresses rapidly, leading to severe complications in just a few days, weeks, months.

Diseases and symptoms

Let us consider in more detail what ailments can develop as a result of such a condition as a disturbed autoimmune process. Symptoms depend entirely on the pathology. Therefore, it is impossible to talk about them separately.

So, if the autoimmune system is disturbed, the following may develop:

Alopecia areata

Hair follicles are attacked. This pathology, as a rule, does not affect the general health. But it significantly worsens the appearance.

The disease is characterized by the following symptoms: there are no patches of hair on the head and other areas of the body.

Autoimmune hepatitis

With this pathology, the immune system destroys the liver. As a result, organ compaction, cirrhosis, and liver failure may occur.

• liver enlargement,
• skin itching,
• weakness,
• jaundice,
• joint pain,
• discomfort in the gastrointestinal tract.

Antiphospholipid syndrome

Against the background of thrombosis of veins and arteries, damage to blood vessels occurs.

The development of such a pathology is indicated by:

• presence of blood clots,
• mesh rash on wrists, knees,
• spontaneous abortions.

Celiac disease

With this pathology, people are gluten intolerant. This is a substance found in rice, grains, and barley. When these foods or certain medications are taken, the system attacks the intestinal lining.

Symptoms:

• pain, bloating;
• upset or constipation;
• weight loss or weight gain;
• weakness, rash, itching on the skin;
• disrupted menstrual cycle, miscarriage, infertility.

Graves' disease

This is a pathology in which a disturbed autoimmune process occurs in the thyroid gland. The affected organ begins to produce a lot of hormones.

The disease is characterized by:

• irritability,
• increased sweating,
• weight loss,
• insomnia,
• trembling hands
• minor menstruation,
• hair section,
• high heat demand
• bulging eyes,
• muscle weakness.

Type 1 diabetes

In this case, those cells that produce insulin are attacked. This hormone ensures normal blood sugar levels. Without insulin, the norm is significantly exceeded. As a result, damage to the heart, kidneys, eyes, teeth, and nerves may occur.

The symptoms of this disease are:

• feeling of thirst,
• feeling tired, hungry,
• itching, dry skin,
• frequent urination,
• poor wound healing,
• involuntary weight loss,
• tingling or loss of sensation in the limbs,
• visual impairment (the image is perceived as blurred).

Multiple sclerosis

Characteristic damage to the nerve sheath. Damage affects the brain and spinal cord. Symptoms vary depending on the extent and area of ​​the lesion.

The following signs may be observed:

• poor coordination, loss of balance, weakness;
• speech problems;
• tremor;
• paralysis;
• tingling, numbness of the limbs.

Psoriasis

The disease develops as a result of the active production of new skin cells in the deep layers. They begin to accumulate on the surface of the epidermis.

The disease manifests itself with the following symptoms:

• red, rough spots that resemble scales;
• they appear on the elbows, knees, head;
• pain and itching appears.

A specific form of arthritis may develop that affects the joints of the fingers. When the sacrum is involved in the process, pain and discomfort occurs in the back.

Hashimoto's disease

This is another disease in which the autoimmune process in the thyroid gland is disrupted. But this pathology is characterized by insufficient production of hormones.

The disease is indicated by:

• fatigue, weakness;
• sudden weight gain;
• increased sensitivity to cold;
• discomfort in muscle tissue;
• poor joint mobility;
• constipation;
• swelling of the face.

Rheumatoid arthritis

The immune system begins to attack the lining of the joints.

The following manifestations are characteristic:

• pain, poor mobility in joints;
• joints become swollen and deformed;
• movements are significantly limited;
• fatigue, fever appears;
• Knob-like subcutaneous formations may be observed, most often on the elbows.

Diagnosis of pathology

How can you determine the development of the disease? In diagnosing diseases, one of the most important points is identifying the immune factor that provoked tissue damage.

In addition, the hereditary factor is taken into account. It is very important to inform your doctor about all symptoms that arise, even those that, at first glance, seem insignificant.

Special tests are required. The autoimmune inflammatory process cannot go unnoticed. It can be detected by testing for antibodies in the blood. Various immunological laboratory examination methods may also be prescribed.

Who to contact?

Quite often, people whose autoimmune processes are disrupted do not know which doctor to visit. This is not surprising, because pathology can affect a variety of systems.

It is best to consult a therapist initially. Depending on which organs are affected, the doctor will refer the patient to a specialist.

This could be: endocrinologist, gastroenterologist, dermatologist, hepatologist, rheumatologist, hematologist, gynecologist, urologist.

In addition, you will need the help of a psychotherapist, psychologist and nutritionist.

Treatment methods

Is it possible to fight this pathology? Today, treatment of the autoimmune process is carried out quite successfully thanks to numerous studies by specialists. When prescribing medications, doctors take into account that the immune system is the main factor that negatively affects the body. Accordingly, therapy is designed to reduce its activity or restore the necessary balance.

For autoimmune diseases, medications are prescribed:

1. Immunosuppressants. Such drugs have a depressing effect on the functioning of the immune system. This category includes: antimetabolites, cytostatics, corticosteroid hormones, some antibiotics. The use of these drugs allows you to stop the inflammatory process and significantly reduce the activity of the immune system. However, immunosuppressants have a number of negative reactions. After all, they affect the entire body. Sometimes hematopoiesis may be impaired, high susceptibility to infection may occur, and internal organs may be affected. That is why these medications can only be prescribed by a doctor, after a complete check of the body. In this case, therapy must be carried out under the supervision of a competent specialist.
2. Immunomodulators. These medications are prescribed to achieve a balance between the various components of the immune system. As a rule, these medications are of natural origin. The most commonly prescribed drugs are: Alfetin, Echinacea purpurea, Rhodiola rosea, Ginseng extract.

Lifestyle

People who have impaired autoimmune processes need to follow certain rules. They will help improve your well-being and reduce the number of exacerbations. But they should be performed regularly.

1. Work with a nutritionist to develop an appropriate diet. Patients need to eat enough vegetables, fruits, low-fat dairy products, whole grains and plant proteins. And it is better to avoid excess sugar, salt, and saturated fats.
2. Play sports. Be sure to discuss with your doctor what kind of activity is recommended for you. Exercise is very beneficial for people suffering from joint and muscle pain.
3. Provide adequate rest. It allows the body to recover. For people who don't get enough sleep, symptom severity and stress levels increase significantly. As a rule, a person needs 7-9 hours for proper rest.
4. Protect yourself from stress. Constant anxiety can lead to an exacerbation of an autoimmune disease. That is why patients need to find methods and techniques to cope with stress. Quite effective techniques are: self-hypnosis, meditation, visualization.

Conclusion

Unfortunately, it is impossible to get rid of an autoimmune disease. But this does not mean that you cannot enjoy life with such an illness. Be sure to follow all the doctor’s recommendations, take the treatment prescribed by him, and visit the doctor according to the prescribed schedule. This will significantly reduce unpleasant symptoms, which means you can continue to enjoy life.