Fas-fas ligand: Checkpoint of t cell functions in multiple sclerosis

Research output: Contribution to journalShort surveypeer-review


Fas and Fas Ligand (FasL) are two molecules involved in the regulation of cell death. Their interaction leads to apoptosis of thymocytes that fail to rearrange correctly their T cell receptor (TCR) genes and of those that recognize self-antigens, a process called negative selection; moreover, Fas-FasL interaction leads to activation-induced cell death, a form of apoptosis induced by repeated TCR stimulation, responsible for the peripheral deletion of activated T cells. Both control mechanisms are particularly relevant in the context of autoimmune diseases, such as multiple sclerosis (MS), where T cells exert an immune response against self-antigens. This concept is well demonstrated by the development of autoimmune diseases in mice and humans with defects in Fas or FasL. In recent years, several new aspects of T cell functions in MS have been elucidated, such as the pathogenic role of T helper (Th) 17 cells and the protective role of T regulatory (Treg) cells. Thus, in this review, we summarize the role of the Fas-FasL pathway, with particular focus on its involvement in MS. We then discuss recent advances concerning the role of Fas-FasL in regulating Th17 and Treg cells' functions, in the context of MS.

Original languageEnglish
Article number382
JournalFrontiers in Immunology
Issue numberSEP
Publication statusPublished - Sep 27 2016


  • Cell death
  • Fas-FasL
  • Multiple sclerosis
  • T regulatory cells
  • Thelper 17 cells

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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