[Mechanisms for B cell tolerance and their defects in systemic autoimmune diseases].
Lines of evidence suggest that self-reactive B cells are deleted or functionally inactivated at the several different steps of maturation from immature B cells to antibody producing cells. These self-tolerance mechanisms appear to involve B cell apoptosis induced by signaling via the antigen receptor (surface immunoglobulin) or Fas. In mice prone to systemic autoimmune diseases such as bcl-2 transgenic, NZB or (NZB x NZW) F1 mice, antigen receptor-mediated B cell apoptosis is defective. In another autoimmunity-prone mice MRL/lpr, autoantibody production requires defects of Fas in B cells. These findings strongly suggest that the defects in B cell tolerance play an important role in the pathogenesis of systemic autoimmune diseases.
Tsubata
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T
Medical Research Institute, Tokyo Medical and Dental University.
D000818:Animals; D017209:Apoptosis; D001327:Autoimmune Diseases / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology*; D006801:Humans; D007108:Immune Tolerance; D051379:Mice; D008815:Mice, Inbred Strains; D011947:Receptors, Antigen, B-Cell / Q000276:immunology; D019014:fas Receptor / Q000276:immunology
D011947:Receptors, Antigen, B-Cell; D019014:fas Receptor