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Studies on T‐cell receptors involved in experimental autoimmune encephalomyelitis using the complementary peptide recognition approach
Author(s) -
Xian C. J.,
Simmons R. D.,
Willenborg D. O.,
Vandenbark A. A.,
Hashim G. A.,
Carnegie P. R.
Publication year - 1995
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490410508
Subject(s) - experimental autoimmune encephalomyelitis , receptor , encephalomyelitis , peptide , neuroscience , immunology , computational biology , multiple sclerosis , chemistry , medicine , biology , biochemistry
Based upon Blalock's complementary recognition approach, a complementary or antisense peptide (CP) was designed to the experimental autoiramune encephalomyelitis (EAE) epitope peptide, rat myelin basic protein (MBP) peptide 72‐82. This peptide (EAE CP) was shown to have some sequence similarities to T‐cell receptors (TCR) and MHC II molecules in a sequence homology search. Solid‐phase binding as‐says demonstrated specific and high affinity binding (3 and 4 μM) between the EAE CP and the rat and guinea pig EAE epitope peptides (Rt72‐82 and Gp69‐82), respectively. This EAE CP was also found to be immunogenic in rats in an ear swelling test for delayed type hypersensitivity (DTH) reactions and an ELISA for antibody responses. However, a rabbit antibody generated to EAE CP was shown to be unable to stain the Vβ8 + EAE susceptible T‐cells in immunofluorescence analyses. This EAE CP was also used in attempts to down‐regulate EAE and the results showed that prior immunization with EAE CP in complete Freund's adjuvant could not prevent the Lewis rats from developing EAE. Although the data on sense‐antisense peptide interaction were positive and the EAE CP was immunogenic, the inability of EAE CP to regulate EAE indicates that the CP approach may not be generally applicable. © 1995 Wiley‐Liss, Inc.