From Big Medical Encyclopedia

AUTOANTIGENS (grech, autos + antigen[s]) — the components of cells and fabrics of own organism which became partially alien under the influence of various disturbing factors and infectious agents or as a result of disturbance of natural unresponsiveness.

Own substances of an organism can get elements of allogeneity and become antigens under the influence of various exogenous factors. Arisen to them autoantibodies (see) can react also with own components which are not changed before because of existence of the general determinant groups at And. and normal fabrics. From experiments it is known that the protective mechanism against viruses can be directed at the same time against cells of the owner acting as the carrier of antigen. Fernandos (M. of Fernandos, 1964) and Rowe (W. P. Rowe, 4967) called this process passive cytotoxicity. It is possible that thus hemolitic anemia, immune leucio-and thrombocytopenia develops.

Autoantibodies can result from so-called gaptenny effect. Chemical agents, communicating as haptens own proteins, become antigens, and antibodies are formed not only against haptens, but also to antigen carrier. In such way, in particular, there is a so-called sedormidny purpura. It is possible to assume that haptens of cells and fabrics can be occluded on microorganisms and cause formation of autoantibodies. On the basis of the gaptenny mechanism in certain cases antibodies are formed to exogenous hapten or to the new determinants which are formed in connection with conjugation of hapten with proteins, but not to normal autologous determinants of protein. The opinion is expressed that such antibodies cannot be referred to category of true autoantibodies though they also play a role in an immunopathology. At the same time emergence of the true autoantibodies directed to normal determinants of the autologous protein which is in a complex with hapten is possible.

The changes caused by chemical and other reasons, perhaps are used as specific antigenic determinants for emergence of autoantibodies. Rather damaging action of autoantibodies on the next structures which thanks to it become effective antigens. In it provocative action of autoantibodies which then can react with the autologous fabric which is not changed before consists.

The provocative role of autoantibodies by formation of cell-bound immune complexes in vessels is of great importance. The circulating antigens and antibodies can form such complex in the smallest vessels, first of all in kidneys, lungs and skin, causing a local inflammation — a so-called immunocomplex vasculitis. The inflammatory changes in fabrics arising in such way quite often can lead to emergence of autoantigens which provoke development of autoantibodies again with their property to cause a self-sustaining inflammation. On the described type some forms of nephrite, damage of internals at a system lupus erythematosus develop and, perhaps, a pseudorheumatism. Besides, in case of dissociation of a complex antigen — an antibody immune globulin can have immunogene effect probably. It is confirmed by frequent detection of an antigammaglobulinovy factor or rhematoid factor at such reactions.

In connection with told there is a question of a role is long the waste products of microbes coming to an organism in developing of autoimmune diseases. It is shown that repeated introduction to rabbits of streptolysin S led to emergence of arthritis with existence of autoantibodies to intracellular components. Data similar in essence are obtained as a result of administration of streptococcal proteinase and other microbic antigens.

Products of exchange of bacteria can probably break an immunological homeostasis so that autologous substances which were available up to this point, but were too weak for formation of the immunological answer, are able to cause formation of autoantibodies. Similar process, as we know, results from introduction of the full Freund's adjuvant consisting of the killed tubercular bacteria.

It is suggested about a role of so-called complex antigens in emergence of autoimmune reactions. Formation of autoantibodies at rheumatism can arise from formation of the complex antigen consisting of the fabrics damaged by heterogeneous cytotoxins and a streptococcus which possesses an adjuvanticity. Various microorganisms are not equivalent on the adjuvanticities.

To establish belonging of this disease to category of autoimmune, special criteria among which release of specific fabric antigen and studying of products of antibodies to it mu to antigen appears are offered. Thus, studying of fabric and serumal components for the purpose of release of antigens, specific to this disease — one of nodal links in a chain of proofs of the autoimmune nature of this disease.

It is suggested that serum of patients with rheumatism, rhematoid arthritis and a system lupus erythematosus contain the antigens characteristic of these diseases. Told is confirmed by the fact that serums of the mentioned groups of patients react more often and stronger with the antiserums of the same name, than serums of clinically healthy people and patients with other diseases. Identification of the antigens characteristic of patients with collagenoses is made by immunoadsorption and other immunological methods that has a certain diagnostic value. Identification of rheumatic antigen in serums of patients with rheumatism in an inactive phase testifies to the minimum activity of process, a cut does not come to light by other methods.

In blood serum of patients with collagenic diseases so-called kollagenopodobny protein comes to light. Its concentration in blood serum of patients makes 100 mkg/ml that exceeds the level of this protein at clinically healthy people by 10 — 12 times and is in direct dependence on activity of process. In gamma-globulins of blood serum of patients with a pseudorheumatism not only quantitative, but also qualitative changes are revealed. In synovial fluid of patients with a pseudorheumatism the special antigens which are absent in serum and in synovial tissue of clinically healthy people are revealed. Besides, in synovial fluid of patients with a pseudorheumatism the so-called vazopressivny factor (P-factor) which is absent in synovial fluid of patients with gouty and psoriasis arthritis and other high-quality shifts is found. All this indicates deep disturbances of exchange at collagenic diseases.

At a system lupus erythematosus and a pseudorheumatism the autoantibodies which are characterized by a certain specificity that has huge value for diagnosis are revealed. Even if the rhematoid factor is also found at some other diseases, it indicates a wide spread occurance of autoimmune mechanisms of development of diseases. Everything told says that during the studying of autoimmune diseases special attention should be paid on specific And. and corresponding autoantibodies (see).

Extremely fruitfully kliniko-immunological research of autoantigens and autoantibodies. E.g., during the studying of so-called rheumatic antigen and cardial autoantibodies in blood serum of patients inertly and latentno the current returnable rheumatic carditis revealed dominance of one of the called factors. It indicates the competitive relations of various indicators which simultaneous definition provides more reliable characteristic of autoimmune process. See also Antigens , Autoallergy .

Bibliography: Gaurovits F. Immunochemistry and biosynthesis of antibodies, the lane with English, M., 1969; Ioffe V. I. Clinical and epidemiological immunology, JI., 1968; Kupchinskas Yu. K. Clinic and immunology of autoallergichesky diseases and medicinal allergy, M. * 1963; Lyampert I. M. Etiology, immunology and immunopathology of rheumatism, M., 1972; V. I Nets. Antigenic properties of serum proteins at some collagenoses, M., 1969, bibliogr.; Dameshek W. Autoimmunity, theoretical aspects, Ann. N. Ύ. Acad. Sei., v. 124, p. 6, 1965; Glynn L.E.a.Hol-b about about w E. J. Autoimmunity and disease, Oxford, 1965; Köhler W.Die Serologie des Rheumatismus und der Streptokokkeninfektionen, Lpz., 1959.

V. I. Sachkov, E. G. Pushkar.