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An autologous self‐antigen differentially regulates expression of I‐A glycoproteins and B7 costimulatory molecules on CD4 − CD8 − T helper cells
Author(s) -
Walker Mindi R.,
White Gregory A.,
Nardella John P.,
Mannie Mark D.
Publication year - 1999
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.66.1.120
Subject(s) - biology , antigen , antigen presenting cell , t cell , major histocompatibility complex , cd8 , cytotoxic t cell , microbiology and biotechnology , immunology , antigen presentation , t lymphocyte , myelin basic protein , immune system , myelin , endocrinology , biochemistry , in vitro , central nervous system
During inflammation, T helper cells transiently express class II major histocompatibility complex (MHC) glycoproteins and present antigens to other T cells. To assess involvement of self‐antigens in the generation of T cell antigen‐presenting cell (T‐APC) activity, rat (R) myelin basic protein (MBP) was used to stimulate a rat CD4 − CD8 − T cell clone. RMBP induced T cell surface expression of class II MHC glycoproteins and T‐APC activity, although RMBP did not elicit interleukin (IL‐2) production or proliferation. When added to culture with the strong agonist guinea pig (GP) MBP, RMBP acted as a partial antagonist and inhibited responses of IL‐2 production, proliferation, and T cell expression of B7.1. RMBP did not, however, efficiently antagonize GPMBP‐induced I‐A expression on T cells. These findings indicate that the self‐antigen RMBP specifically induces accumulation of I‐A/peptide complexes at signaling thresholds that inhibit pathogenic autoimmune responses. Overall, this study suggests a role for self‐antigens in the generation of B7‐deficient T‐APC activity as a mechanism of tolerance in experimental autoimmune encephalomyelitis. J. Leukoc. Biol. 66: 120–126; 1999.