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pubmed-article:10410999pubmed:abstractTextDuring 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.lld:pubmed
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pubmed-article:10410999pubmed:authorpubmed-author:WhiteG AGAlld:pubmed
pubmed-article:10410999pubmed:authorpubmed-author:WalkerM RMRlld:pubmed
pubmed-article:10410999pubmed:authorpubmed-author:MannieM DMDlld:pubmed
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pubmed-article:10410999pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:10410999pubmed:articleTitleAn autologous self-antigen differentially regulates expression of I-A glycoproteins and B7 costimulatory molecules on CD4- CD8- T helper cells.lld:pubmed
pubmed-article:10410999pubmed:affiliationDepartment of Microbiology and Immunology, East Carolina University School of Medicine, Greenville, North Carolina 27858-4354, USA.lld:pubmed
pubmed-article:10410999pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:10410999pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed