Pathogenic mechanisms in autoimmune diseases.
Autoimmunity may be initiated by a variety of mechanisms involving changes in autologous antigens or alterations in immune regulation. Autoimmune disease, the pathological consequence of an autoimmune response, depends principally upon the stimulation of helper/inducer T cells reactive with self-antigens. Such T cells direct the quantity and quality of the immune response by influencing the mixture of interleukins produced. Autoantibodies react with accessible cells and mediate injury directly or indirectly. Delayed hypersensitivity reactions indirectly damage tissues through the agency of lymphokines. Cytotoxic T cells penetrate tissue spaces and attack cells bearing requisite surface antigens complexed with the appropriate major histocompatibility complex product. Macrophages and NK cells, activated by lymphokines, have potential to augment tissue damage. These several mechanisms do not operate in isolation; rather, multiple processes act in unison in most autoimmune diseases.
Rose
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Johns Hopkins University, Department of Immunology & Infectious Diseases, Baltimore, Maryland 21205.
D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology; D001323:Autoantibodies / Q000096:biosynthesis; D001324:Autoantigens / Q000276:immunology; D006801:Humans; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007111:Immunity, Cellular; D008285:Major Histocompatibility Complex; D009205:Myocarditis / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D013967:Thyroiditis, Autoimmune / Q000276:immunology*
D001323:Autoantibodies; D001324:Autoantigens