Role of Fas-FasL interactions in the pathogenesis and regulation of autoimmune demyelinating disease

Kimberly A. Sabelko-Downes, John H. Russell, Anne H. Cross

Research output: Contribution to journalArticle

46 Scopus citations

Abstract

Multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) represent complex processes that lead to destruction of oligodendrocytes (ODCs) and myelin. T cells are integral to the development of these diseases, but whether T cell-mediated cytolytic mechanisms are involved in the destruction of MHC Class II-negative targets, such as oligodendroglia and myelin, in the CNS is unclear. The primary lytic mechanism employed by CD4+ T cells is Fas-dependent, but can be MHC-unrestricted. Thus, T cell-mediated Fas-FasL interactions could directly contribute to the pathology of EAE and MS. This review summarizes studies from our laboratory and others that implicate Fas-FasL interactions in both the pathogenesis and regulation of demyelinating diseases. Copyright (C) 1999 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)42-52
Number of pages11
JournalJournal of Neuroimmunology
Volume100
Issue number1-2
DOIs
StatePublished - Dec 1999

Keywords

  • Apoptosis
  • Autoimmunity
  • Demyelinating disease
  • Inflammation
  • T cell regulation

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