Class II major histocompatibility antigens and the etiology of systemic lupus erythematosus.
It is hypothesized that the underlying immunoregulatory dysfunction in systemic lupus erythematosus (SLE) is altered recognition by T cells of self class II major histocompatibility antigens (Ia). The resultant cellular autoreactivity would directly cause certain of the immunopathological manifestations of SLE. The perception by T cells of self non-MHC antigens in the context of altered Ia on antigen presenting cells would also stimulate specific help for autoantibody production. Autoimmunity induced by the graft-versus-host reaction is an experimental model that illustrates this potential mechanism (A. G. Rolink, S. T. Pals, and E. Gleichmann, J. Exp. Med. 157, 755, 1983; R. A. Eisenberg, S. Y. Craven, and P. L. Cohen, Arth. Rheum. 26, S19, 1983).
D001402:B-Lymphocytes / Q000276:immunology; D005802:Genes, MHC Class II; D006649:Histocompatibility Antigens / Q000235:genetics*; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000209:etiology / Q000276:immunology*; D008285:Major Histocompatibility Complex; D013601:T-Lymphocytes / Q000276:immunology*
D006649:Histocompatibility Antigens