Class II major histocompatibility antigens and the etiology of systemic lupus erythematosus

Clinical Immunology and Immunopathology
R A Eisenberg, P L Cohen

Abstract

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).

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Citations

Jun 19, 2012·Journal of Autoimmunity·Robert A Eisenberg, Charles S Via
Feb 28, 1998·Immunologic Research·R Eisenberg
Mar 3, 2007·Nihon Rinshō Men'eki Gakkai kaishi = Japanese journal of clinical immunology·Daitaro Kurosaka
Nov 4, 2006·The Journal of Immunology : Official Journal of the American Association of Immunologists·Zhongjie MaRobert A Eisenberg
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