Fas-Fas Ligand: Checkpoint of T Cell Functions in Multiple Sclerosis

• Published in: Frontiers in immunology 2016-09, Vol.7, p.382-382
• Main Authors: Volpe, Elisabetta, Sambucci, Manolo, Battistini, Luca, Borsellino, Giovanna
• Format: Article
• Language: English
• Subjects: Cell Death; Fas-FasL; Immunology; Multiple Sclerosis; T regulatory cells; Thelper 17 cells
• ISSN: 1664-3224; 1664-3224
• DOI: 10.3389/fimmu.2016.00382

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.