Degenerate antigen recognition by CD4+ effector T cells in experimental autoimmune encephalomyelitis

Bradford L. McRae, Nitin J. Karandikar, Stephen D. Miller

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

Peptide-specific tolerance with PLP139-151 peptide analogs was used to compare the fine antigen-specificity requirements at both the inductive and effector phases of relapsing EAE (R-EAE). A PLP139-151 analog peptide containing a single substitution at the primary T cell receptor (TcR) contact residue (A144) did not induce proliferation in PLP139-151-primed CD4+ T cells. In addition, tolerance induced with ECDI-treated, A144-coupled splenocytes failed to prevent the inductive phase of PLP139-151-induced R-EAE or to inhibit the induction of peptide-specific DTH indicating that naive PLP139-151-specific T cells do not react with the A144 peptide analog. In contrast, A144-coupled splenocytes did prevent the expression of the effector phase of R-EAE and inhibited the elicitation of peptide-specific DTH responses upon administration to mice seven days after immunization with PLP139-151. The results provide in vivo evidence that 'antigen-experienced' T cells recognize a broader repertoire of antigens than do naive T cells and have important implications for the regulation of immune responses and for advancing our understanding of the pathogenesis and treatment of autoimmune disease.

Original languageEnglish (US)
Pages (from-to)156-162
Number of pages7
JournalJournal of Neuroimmunology
Volume75
Issue number1-2
DOIs
StatePublished - May 1997

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Keywords

  • altered peptide ligands
  • cytokines
  • encephalitogenic peptide
  • experimental autoimmune encephalomyelitis
  • proteolipid protein
  • SJL/J mice

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

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