A potential role for Fas (CD95/APO-1) in the recovery phase of relapsing - Remitting Experimental Autoimmune Encephalomyelitis (EAE)

Graig C. Suvannavejh*, Stephen D Miller

*Corresponding author for this work

Research output: Contribution to journalArticle

Abstract

EAE is a CD4+ Th1 inflammatory disease of the central nervous system that is used as a model for the human demyelinating disease multiple sclerosis. SJL mice that are induced with EAE often exhibit a relapsing and remitting disease course, one that is similar to that seen in MS patients. While many of the salient features of this model have been elucidated, the exact mechanisms of disease remission in these animals remain poorly understood. Fas is a 45kD cell surface protein that is a member of the TNF receptor family and has been shown to be a critical mediator of cellular apoptosis and activation-induced cell death (AICD). One possibility to account for spontaneous remission in EAE is the AICD of disease-initiating T cells. To investigate this possibility, and in particular the potential role of Fas, Fas-mutant SJL mice were immunized with PLP 139-151, the immunodominant epitope on the PLP protein, in CFA. While control Fas +/+ wild-type SJL and Fas +/- mice exhibited the characteristic relapsing-remitting disease course with each animal entering remission following the acute phase of disease, a majority of the sick Fas-/- never entered remission. In fact, these Fas -/- animals never recovered, and eventually succumbed to the disease, whereas no Fas +/- or Fas +/+ mice died. These results suggest that Fas/FasL interactions may be critical in regulating events following the acute phase of disease and may represent an intrinsic regulatory mechanism for the remission from disease that is observed in normal SJL mice.

Original languageEnglish (US)
JournalFASEB Journal
Volume12
Issue number5
StatePublished - Mar 20 1998

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

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