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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.

Authors
  • Walker, M R
  • White, G A
  • Nardella, J P
  • Mannie, M D
Type
Published Article
Journal
Journal of Leukocyte Biology
Publisher
Wiley
Publication Date
Jul 01, 1999
Volume
66
Issue
1
Pages
120–126
Identifiers
PMID: 10410999
Source
Medline
License
Unknown

Abstract

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.

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