Castro J E, Listman J A, Jacobson B A, Wang Y, Lopez P A, Ju S, Finn P W, Perkins D L
Pulmonary Division, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
Immunity. 1996 Dec;5(6):617-27. doi: 10.1016/s1074-7613(00)80275-7.
A major mechanism maintaining immune tolerance is the deletion of potentially autoreactive thymocytes by apoptosis during development in the thymus. Previous reports suggest that apoptosis is induced by high avidity signals transduced via the T cell receptor; however, the role of signals transduced by other cell surface receptors during thymic selection remains poorly understood. Fas, a member of the TNF receptor family, has been shown to induce apoptosis in mature peripheral T cells; however, the effects of Fas on negative selection of thymocytes have not been previously detected. Using a sensitive terminal deoxynucleotidyl transferase method to detect apoptotic cells, we found that mutant Fas molecules in lpr mice decrease the sensitivity of thymocytes to T cell receptor-mediated apoptosis and that blockade of Fas-Fas ligand interactions in vivo can inhibit antigen-induced apoptosis of thymocytes in non-lpr mice. Thus, we have shown that Fas, in conjunction with antigen-specific signals, can modulate apoptosis during negative selection of thymocytes.
维持免疫耐受的一个主要机制是在胸腺发育过程中通过凋亡清除潜在的自身反应性胸腺细胞。先前的报道表明,凋亡是由通过T细胞受体转导的高亲和力信号诱导的;然而,在胸腺选择过程中,其他细胞表面受体转导的信号所起的作用仍知之甚少。Fas是TNF受体家族的成员,已被证明可诱导成熟外周T细胞凋亡;然而,此前尚未检测到Fas对胸腺细胞阴性选择的影响。我们使用一种敏感的末端脱氧核苷酸转移酶方法来检测凋亡细胞,发现lpr小鼠中的突变Fas分子降低了胸腺细胞对T细胞受体介导的凋亡的敏感性,并且体内阻断Fas-Fas配体相互作用可抑制非lpr小鼠中抗原诱导的胸腺细胞凋亡。因此,我们已经表明,Fas与抗原特异性信号一起,可以在胸腺细胞阴性选择过程中调节凋亡。