Lymphokines in autoimmunity--roles of interferons in systemic lupus erythematosus and other autoimmune disorders.
All healthy subjects have the capacity to produce autoantibodies markedly similar to those seen in autoimmune disease. This capacity may be activated by viruses, through the release of IFN or other mechanisms. Autoimmune disease can be induced or enhanced by interferons in mice and in humans. Circulating IFNs are very frequent in patients with autoimmune diseases and may participate in the mediation of several clinical and immunologic manifestations. IFN-induced aberrant HLA-DR expression is common on epithelial cells of target organs of many autoimmune diseases; it may present autoantigen to T-cells and initiate a cycle of self-perpetuating autoimmunity. Interaction of IFN with other lymphokines (TNF, interleukin 1, etc.) may contribute to disease development. Further understanding of the role of lymphokines in autoimmunity may provide the basis for specific therapy in the future.
Schattner
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Department of Medicine, Kaplan Hospital, Rehovot, Israel.
D000818:Animals; D001323:Autoantibodies / Q000096:biosynthesis*; D001327:Autoimmune Diseases / Q000209:etiology / Q000276:immunology*; D006684:HLA-DR Antigens / Q000276:immunology; D006801:Humans; D007130:Immunoglobulin Idiotypes / Q000096:biosynthesis; D007372:Interferons / Q000494:pharmacology; D008180:Lupus Erythematosus, Systemic / Q000276:immunology; D008222:Lymphokines / Q000494:pharmacology*; D051379:Mice; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D001323:Autoantibodies; D006684:HLA-DR Antigens; D007130:Immunoglobulin Idiotypes; D008222:Lymphokines; D014409:Tumor Necrosis Factor-alpha; D007372:Interferons