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Antibodies specific for VB8 receptor peptide suppress experimental autoimmune encephalomyelitis.

作者信息

Hashim G A, Vandenbark A A, Galang A B, Diamanduros T, Carvalho E, Srinivasan J, Jones R, Vainiene M, Morrison W J, Offner H

机构信息

Department of Microbiology, St. Luke's-Roosevelt Hospital, New York, NY 10025.

出版信息

J Immunol. 1990 Jun 15;144(12):4621-7.

PMID:1693637
Abstract

Recent studies from our laboratory have shown, for the first time, that a synthetic peptide from that TCR VB chain used preferentially by encephalitogenic T cells induced the formation of protective, MHC class I-restricted T cells and prevented the development of EAE in Lewis rats. In this report we 1) demonstrate that immunization with the TCR-VB8-39-59 peptide generated peptide-specific antibodies that protect against experimental autoimmune encephalomyelitis induced by either of the two distinct encephalitogenic epitopes of basic protein, and 2) characterize the production and biologic functions of rat and rabbit antibody responses to the TCR peptide. The antibodies in both species increased in titer over time, were highly specific for the immunogen by direct reaction and inhibition assays, stained only VB8+ T cells, and suppressed clinical signs and to lesser extent the number of histologic lesions of experimental autoimmune encephalomyelitis mediated by VB8+ T cells. Coupled with our previous work, these results indicate that both humoral and cellular responses to the TCR-VB8-39-59 peptide can contribute independent immunoregulatory effects on encephalitogenic T lymphocytes that use common V region genes in response to epitopes of myelin basic protein.

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