Wang J, Watanabe T
Department of Molecular Immunology, Kyushu University, Fukuoka, Japan.
Int Rev Immunol. 1999;18(4):367-79. doi: 10.3109/08830189909088489.
Fas (Apo-1, CD95) cell surface antigen belongs to the tumor necrosis factor receptor family and mediates apoptosis of a variety of cell types, including lymphocytes, after ligation with Fas ligand (FasL). Recent studies on the role of Fas/FasL interaction in the immune responses strongly suggest the relevance of dysregulation in Fas-mediated apoptosis as a cause of autoimmune disorders. While Fas is not an essential molecule in the elimination or functional inactivation (anergy) of autoreactive B cells, it is indispensable to the maintenance of peripheral tolerance and prevention of autoimmunity. Studies in the past few years have begun to reveal the mechanism by which susceptibility to Fas-mediated apoptosis in B cells is regulated to allow antigen-specific B cells survive and differentiate and to eliminate nonspecifically activated, potentially selfreactive B cells.
Fas(Apo-1,CD95)细胞表面抗原属于肿瘤坏死因子受体家族,在与Fas配体(FasL)结合后,介导包括淋巴细胞在内的多种细胞类型的凋亡。最近关于Fas/FasL相互作用在免疫反应中作用的研究强烈表明,Fas介导的凋亡失调与自身免疫性疾病的发生有关。虽然Fas在自身反应性B细胞的清除或功能失活(无反应性)中不是必需分子,但它对于维持外周耐受性和预防自身免疫却是不可或缺的。过去几年的研究已开始揭示调节B细胞对Fas介导凋亡易感性的机制,以使抗原特异性B细胞存活和分化,并清除非特异性激活的、潜在的自身反应性B细胞。