Molecular mechanisms of autoimmunity.
Autoimmune diseases result from a combination of genetic susceptibility factors and exogenous influences such as infection or chemical (including drug) exposure. Germline DNA variations in genetic type as well as defects in antigen recognition acquired during thymic education of developing T-lymphocytes both contribute to impaired self: nonself discrimination and set the stage for later development of such diseases as myasthenia gravis, polymyositis, or systemic lupus erythematosus. In addition, drugs such as D-penicillamine, hydralazine, procainamide, or quinidine induce T-cell or B-cell changes which precipitate auto-reactivity and cause drug-induced disease. Intervention in autoimmune diseases with prednisone, alkylating agents or the future use of more selective monoclonal antibody reagents may be life-saving in some of these disorders.
Smiley
J D
JD
Department of Medicine, University of Texas Health Science Center, Southwestern Medical School, Dallas.
Moore
S E
SE
D000974:Antibodies, Antinuclear / Q000276:immunology; D001323:Autoantibodies / Q000276:immunology; D001327:Autoimmune Diseases / Q000209:etiology* / Q000235:genetics / Q000276:immunology / Q000628:therapy; D001402:B-Lymphocytes / Q000276:immunology; D004247:DNA / Q000276:immunology; D006801:Humans; D007130:Immunoglobulin Idiotypes / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000235:genetics / Q000276:immunology; D009157:Myasthenia Gravis / Q000139:chemically induced / Q000276:immunology; D009220:Myositis / Q000139:chemically induced / Q000276:immunology; D010396:Penicillamine / Q000009:adverse effects; D013601:T-Lymphocytes / Q000276:immunology
D000974:Antibodies, Antinuclear; D001323:Autoantibodies; D007130:Immunoglobulin Idiotypes; D004247:DNA; D010396:Penicillamine