Studies on T‐cell receptors involved in experimental autoimmune encephalomyelitis using the complementary peptide recognition approach

C. J. Xian, R. D. Simmons, D. O. Willenborg, A. A. Vandenbark, G. A. Hashim, P. R. Carnegie

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)620-627
Number of pages8
JournalJournal of Neuroscience Research
Volume41
Issue number5
DOIs
StatePublished - Aug 1 1995
Externally publishedYes

Keywords

  • EAE
  • MBP
  • antisense peptide
  • sequence homology

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

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