AN ALPHA-CHAIN TCR CDR3 PEPTIDE CAN ENHANCE EAE INDUCED BY MYELIN BASIC-PROTEIN OR PROTEOLIPID PROTEIN

Citation
T. Yamamura et al., AN ALPHA-CHAIN TCR CDR3 PEPTIDE CAN ENHANCE EAE INDUCED BY MYELIN BASIC-PROTEIN OR PROTEOLIPID PROTEIN, Journal of neuroscience research, 45(6), 1996, pp. 706-713
Citations number
36
Categorie Soggetti
Neurosciences
ISSN journal
03604012
Volume
45
Issue
6
Year of publication
1996
Pages
706 - 713
Database
ISI
SICI code
0360-4012(1996)45:6<706:AATCPC>2.0.ZU;2-Z
Abstract
Regulation of experimental autoimmune encephalomyelitis (EAE) can be i nduced by anti-idiotype immunity against T cell receptor (TCR) fragmen ts associated with major histocompatibility complex (MHC) molecules, H owever, we have recently found that preimmunization with an alpha-chai n TCR CDR3 peptide (LYFCAARSNYQL) derived from myelin basic protein (M BP)-specific clones did not suppress but rather augmented the severity of EAE induced by MBP-specific T cells in SJL/J mice. To test whether CDR3 vaccination could control only a highly restricted T cell popula tion, we studied the effect of the peptide against EAE induced by T ce lls specific for different Ag/MHC ligands and autoimmune diseases affe cting non-neural tissues, In contrast to expectations, the peptide was found to augment not only EAE induced by MBP-specific T cells, but al so proteolipid protein (PLP)-specific T cell- or PLP peptide-induced E AE in SJL/J mice, and MBP-induced EAE and adjuvant arthritis (AA) in r ats. The CDR3 peptide was neither inhibitory nor supportive for Ag-ind uced activation of an encephalitogenic clone in vitro. In addition, th e peptide treatment neither inhibited the induction of Ag-specific T c ells nor altered the APC function of spleen cells. These findings, on the one hand, confirm previous results showing TCR peptide-induced enh ancement of the disease and, on the other hand, indicate that the TCR CDR3 peptide may control T cells with broader Ag/MHC specificities tha n could be expected, Structural similarity among TCR idiotypes of auto immune T cells may partly account for these results. (C) 1996 Wiley-Li ss, Inc.