An α-chain TCR CDR3 peptide can enhance EAE induced by myelin basic protein or proteolipid protein
✍ Scribed by T. Yamamura; T.-C. Geng; M.F. Kozovska; K. Yokoyama; I.R. Cohen; T. Tabira
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 755 KB
- Volume
- 45
- Category
- Article
- ISSN
- 0360-4012
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✦ Synopsis
Regulation of experimental autoimmune encephalomyelitis (EAE) can be induced by anti-idiotype immunity against T cell receptor (TCR) fragments associated with major histocompatibility complex (MHC) molecules. However, we have recently found that preimmunization with an a-chain TCR CDR3 peptide (LYFCAARSNY QL) derived from myelin basic protein (MBP)-specific clones did not suppress but rather augmented the severity of EAE induced by MBP-specific T cells in SJLlJ mice. To test whether CDR3 vaccination could control only a highly restricted T cell population, we studied the effect of the peptide against EAE induced by T cells specific for different Ag/MHC ligands and autoimmune diseases affecting non-neural tissues. In contrast to expectations, the peptide was found to augment not only EAE induced by MBP-specific T cells, but also proteolipid protein (PLP)-specific T cell-or PLP peptide-induced EAE in SJL/J mice, and MBP-induced EAE and adjuvant arthritis (AA) in rats. The CDR3 peptide was neither inhibitory nor supportive for Ag-induced activation of an encephalitogenic clone in vitro. In addition, the peptide treatment neither inhibited the induction of Ag-specific T cells nor altered the APC function of spleen cells. These findings, on the one hand, confirm previous results showing TCR peptideinduced enhancement of the disease and, on the other hand, indicate that the TCR CDR3 peptide may control T cells with broader AglMHC specificities than could be expected. Structural similarity among TCR idiotypes of autoimmune T cells may partly account for these results.