[Immunological pathogenesis of collagenosis].
The present paper contains an analysis of the essential factors which combine in the pathogeny of autoimmune illnesses, using Systemic Erythematous Lupus as a prototype. These patients present a hyperfunction of B lymphocytes due to either an intrinsic defect of these cells or disorders in the cells which regulate them which is translated into a high response to nuclear and lymphocytary antigens. The formation of circulating immunocomplexes in these patients would be responsible for the inflammatory vascular and tissue lesions which they present when the Complement is deposited and activated. The antilymphocyte antibodies affect both the B as well as T lymphocytes, by activating the former and destroying the latter particularly the underpopulation of suppressing T lymphocytes. This is translated into a greater activity of the cells which produce antibodies.
D000818:Animals; D000917:Antibody Formation; D001323:Autoantibodies / Q000276:immunology; D001327:Autoimmune Diseases / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology; D003095:Collagen Diseases / Q000276:immunology*; D004195:Disease Models, Animal; D006801:Humans; D007111:Immunity, Cellular; D008180:Lupus Erythematosus, Systemic / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008814:Mice, Inbred NZB / Q000276:immunology; D051381:Rats; D013601:T-Lymphocytes / Q000276:immunology
D001323:Autoantibodies
Patogenia inmunológica de las colagenosis.