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

J Neuroimmunol. 1999 Dec;100(1-2):42-52. doi: 10.1016/s0165-5728(99)00191-5.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cell Death / immunology
  • Demyelinating Autoimmune Diseases, CNS / immunology*
  • Demyelinating Diseases / immunology
  • Encephalomyelitis, Autoimmune, Experimental / immunology
  • Fas Ligand Protein
  • Humans
  • Membrane Glycoproteins / metabolism*
  • Mice
  • Mice, Inbred MRL lpr
  • Mice, Transgenic
  • Models, Immunological
  • Multiple Sclerosis / immunology
  • Myelin Sheath / immunology
  • Oligodendroglia / metabolism
  • T-Lymphocytes / immunology
  • fas Receptor / metabolism*


  • FASLG protein, human
  • Fas Ligand Protein
  • Fasl protein, mouse
  • Membrane Glycoproteins
  • fas Receptor