Targeting T cells responsive to the priming epitope prevent the relapsing phase of experimental autoimmune encephalomyelitis

Keith W. Wegmann, H. G.Archie Bouwer, Cynthia R. Gregory, Ruth H. Whitham, David J. Hinrichs

Research output: Contribution to journalArticle

1 Scopus citations

Abstract

Upon recovery from the initial episode of experimental autoimmune encephalomyelitis (EAE), virtually all SJL mice develop relapsing/remitting episodes of disease. These relapses may occur due to the reactivation of memory T cells initially stimulated as part of the disease-inducing protocol or naïve T-cell populations stimulated by distinct encephalitogens derived from the inflammatory disease process (epitope spread). We have used encephalitogen-specific non-linear peptide octamers to modify the course of relapsing EAE (rEAE) in SJL mice immunized with an oliogodendrocyte-specific protein peptide (OSP 55-71). Our studies show that the peptide-octamers, which target the T cells stimulated by the priming encephalitogen, but not other candidate encephalitogens, prevent rEAE.

Original languageEnglish (US)
Pages (from-to)74-81
Number of pages8
JournalJournal of Neuroimmunology
Volume260
Issue number1-2
DOIs
StatePublished - Apr 22 2013

Keywords

  • Epitope spread
  • Memory cells
  • Non-linear peptide octamers
  • Peptide immunotherapy
  • Relapsing EAE

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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