Epitope spreading and molecular mimicry as triggers of autoimmunity in the Theiler's virus-induced demyelinating disease model of multiple sclerosis

J. Ludovic Croxford, Julie K. Olson, Stephen D. Miller*

*Corresponding author for this work

Research output: Contribution to journalReview article

65 Scopus citations

Abstract

The pathogenesis of multiple sclerosis (MS), a human demyelinating disease of the central nervous system (CNS), is currently unknown. It is widely thought that MS is an autoimmune disease which is supported by animal studies showing that myelin-specific CD4+ T cells can induce similar clinical disease in mice as observed in MS. However, the mechanism(s) of activation of these autoreactive CD4+ T cells are unknown. Although genetic susceptibility is important, other factors may be involved. Viral infections have long thought to be involved in the pathogenesis of MS although there exists little or no direct evidence implicating a role for a specific virus in MS pathogenesis. This review will discuss two models of virus-induced CNS autoimmunity, molecular mimicry and epitope spreading. These two mechanisms of activation of autoreactive T cells are presented in the context of MS.

Original languageEnglish (US)
Pages (from-to)251-260
Number of pages10
JournalAutoimmunity Reviews
Volume1
Issue number5
DOIs
StatePublished - Oct 1 2002

Keywords

  • Autoimmunity
  • Epitope spread
  • Molecular mimicry
  • Multiple sclerosis
  • Theiler's murine encephalomyelitis virus

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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