作者: J. Skowronski , C. Jolicoeur , S. Alpert , D. Hanahan
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摘要: The failure to induce self-tolerance of simian virus 40 large tumor antigen (T antigen) expressed in the pancreatic beta cells transgenic mice results an autoimmune response against this protein and that synthesize it. In every mouse with delayed onset T-antigen expression consequent nontolerance, B cells, T macrophages are attracted infiltrate islets. contrast, incidence, onset, intensity B-cell produce anti-T-antigen autoantibodies vary considerably genetic background. Thus initial attraction lymphocytes synthesizing a non-self can be separated from activation Haplotypes major histocompatibility complex (MHC) differentially influence character response, H-2d H-2k conferring high incidence humoral autoimmunity. Additional non-MHC linked genes also implicated control response.