Amelioration of EAE by a cryptic epitope of myelin oligodendrocyte glycoprotein

Jeri A. Lyons, Melissa M. Riter, Alaa M. Almatrook, Michael J. Ramsbottom, Anne H. Cross

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Previous work demonstrated that EAE induced by recombinant human MOG was B cell-dependent. Data presented here reveal a T cell response to MOG61–85 in human rMOG-immunized B cell−/− mice not observed in WT mice. Further study revealed this peptide to be a cryptic epitope in WT mice. Co-immunization of B cell−/− mice with MOG35–55 and MOG61–85 peptides led to less severe disease compared to mice immunized with MOG35–55 alone. Disease amelioration was associated with decreased production of Interferon-γ by lymph node cells. Thus, MOG61–85 represents a protective epitope to human rMOG induced EAE in B cell−/− mice.

Original languageEnglish
Pages (from-to)66-73
Number of pages8
JournalJournal of Neuroimmunology
Volume300
DOIs
StatePublished - Nov 15 2016

Keywords

  • Antibody
  • B cells
  • Experimental autoimmune encephalomyelitis
  • Immune regulation
  • Myelin oligodendrocyte glycoprotein
  • T cell epitopes

Fingerprint

Dive into the research topics of 'Amelioration of EAE by a cryptic epitope of myelin oligodendrocyte glycoprotein'. Together they form a unique fingerprint.

Cite this