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

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

Research output: Contribution to journalArticle

1 Citation (Scopus)

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 - 2013

Fingerprint

Autoimmune Experimental Encephalomyelitis
Epitopes
T-Lymphocytes
Peptides
Recurrence
Population
Proteins

Keywords

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

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

Cite this

Targeting T cells responsive to the priming epitope prevent the relapsing phase of experimental autoimmune encephalomyelitis. / Wegmann, Keith W.; Bouwer, H. G Archie; Gregory, Cynthia; Whitham, Ruth; Hinrichs, David J.

In: Journal of Neuroimmunology, Vol. 260, No. 1-2, 2013, p. 74-81.

Research output: Contribution to journalArticle

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