TNF, apoptosis and autoimmunity: A common thread?

被引:68
作者
Beutler, B
Bazzoni, F
机构
[1] Univ Texas, SW Med Ctr, Howard Hughes Med Inst, Dallas, TX 75235 USA
[2] Univ Texas, SW Med Ctr, Dept Internal Med, Dallas, TX 75235 USA
[3] Univ Verona, Dept Gen Pathol, I-37100 Verona, Italy
关键词
cytokine; tumor necrosis factor; Fas ligand; receptor; autoimmunity;
D O I
10.1006/bcmd.1998.0187
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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. (C) 1998 Academic Press.
引用
收藏
页码:216 / 230
页数:15
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