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diseases based on immunity reactions to one’s own organs or tissues.
Autoimmune diseases differ according to their mechanism of origin. One group consists of diseases that result from penetration of the blood vessel-tissue barrier and liberation of physiologically isolated antigens, which may be brain, thyroid, crystalline lens, spermatozoon, and other kinds of tissue. The body does not possess natural resistance (tolerance) to these antigens and responds to them with an immune reaction and the formation of immune lymphocytes and antibodies. Such diseases may be encephalomyelitis, Hashimoto’s disease (diffuse infiltration of the thyroid gland by lymphoid cells with increasing signs of thyrotoxicosis— that is, poisoning by the hormone thyroxin; first described by the Japanese scientist H. Hashimoto in 1912), endophthalmitis (inflammation of the internal structures of the eye), uveitis (inflammation of the vascular or uveal tract of the eye), aspermatogenesis (cessation of production of spermatozoa), pancreatitis, and Addison’s disease.
A second group includes diseases caused by the alteration of one’s own tissue components by physical, chemical, microbial, viral, and other factors. The properties of these tissues are so altered that the body perceives them as foreign. Many autoimmune blood diseases (anemia, leukopenia, thrombocytopenia) are due to the ability of some antigens entering from outside the body, or exoantigens (for example, drugs or bacterial toxins), to become fixed on the surface of cells by simple adsorption or by the formation of complex antigens that retain the antigenic properties of the constituents of the complex. Antibodies that are directed against exoantigens injure the corresponding cells. As the body’s own tissue components react with exoantigens (for example, viruses), intermediate antigens may be formed with new antigenic properties that did not exist in the reacting substances. Several diseases of the central nervous system develop in this fashion.
A third group combines diseases that develop as a result of the affinity of the body’s tissue components with exoantigens. In these diseases the immunological reaction caused by the exoantigen may be directed against the body’s own tissues.
A fourth group of autoimmune diseases includes those resulting from dysfunction of lymphoid tissue itself, causing the appearance of cells that destroy the body’s own tissues. This impairment of the immunological apparatus is probably related either to the genetic characteristics of the organism or to increased mutation (stable changes) of lymphoid cells produced by unfavorable external factors (chemical substances, radiation, etc.). Systemic lupus erythematosus is an example of such an autoimmune disease.
The mechanism of development of many autoimmune diseases (systemic scleroderma, periarteritis nodosa, acquired hemolytic anemia, etc.) is obscure. Most of them develop as allergic reactions of the delayed type with the participation of immune lymphocytes. Antibodies circulating in the blood are of primary importance in autoimmune diseases affecting the blood.
REFERENCESCriep, L. Klinicheskaia immunologiia i allergiia. Moscow, 1966. (Translated from English.)
Immunopatologiia v KLinike i eksperimente i problema autoantitel. Moscow, 1963.(Translated from German.)
A. KH. KANCHURIN