Beutler B, Bazzoni F
Howard Hughes Medical Institute, University of Texas Southwestern Medical Center at Dallas 75235-9050, USA.
Blood Cells Mol Dis. 1998 Jun;24(2):216-30. doi: 10.1006/bcmd.1998.0187.
A subset of cytokine mediators belonging to the tumor necrosis factor (TNF) family cause apoptosis, acting through receptors and signaling pathways that have recently come to light. Further, at least one autoimmune disease results from a defined defect of apoptosis (mutations of the Fas ligand or its receptor). It is offered that many, and perhaps most autoimmune diseases may result from primary defects of apoptosis. Such defects may cause reflexive overproduction of TNF and other pro-apoptotic cytokines. The collateral damage produced by these mediators may be of pathogenetic importance in complex autoimmune disorders such as rheumatoid arthritis and Crohn disease, wherein TNF blockade is known to have ameliorative effects.
属于肿瘤坏死因子（TNF）家族的一部分细胞因子介质可通过最近才被发现的受体和信号通路引发细胞凋亡。此外，至少有一种自身免疫性疾病是由细胞凋亡的明确缺陷（Fas配体或其受体的突变）导致的。有人认为，许多甚至可能大多数自身免疫性疾病可能是由细胞凋亡的原发性缺陷引起的。这些缺陷可能导致TNF和其他促凋亡细胞因子的反射性过度产生。在类风湿性关节炎和克罗恩病等复杂的自身免疫性疾病中，这些介质造成的附带损害可能在发病机制上具有重要意义，已知在这些疾病中TNF阻断具有改善作用。
