Gupta Sudhir
Division of Basic and Clinical Immunology, University of California, Irvine 92697, USA.
J Clin Immunol. 2002 Jul;22(4):185-94. doi: 10.1023/a:1016089607548.
Tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine, exerts its biological activity by signaling via its two receptors, TNF-RI and TNF-RII, and by activating NF-kappaB. NF-kappaB is essential for survival of many cell types; however, TNF-alpha also induces cell death. In this article, both the survival and cell death signaling by TNF-alpha and the role of caspases in turning off NF-kappaB survival signal are reviewed. Furthermore, a role of DAP kinase in TNF-induced apoptosis is discussed. Finally, the molecular basis of the effect of age on TNF-alpha-induced apoptosis in human T cells is reviewed.
肿瘤坏死因子-α（TNF-α）是一种促炎细胞因子，通过其两种受体TNF-RI和TNF-RII进行信号传导并激活核因子κB（NF-κB）来发挥其生物学活性。NF-κB对许多细胞类型的存活至关重要；然而，TNF-α也会诱导细胞死亡。在本文中，我们综述了TNF-α的存活和细胞死亡信号传导以及半胱天冬酶在关闭NF-κB存活信号中的作用。此外，还讨论了DAP激酶在TNF诱导的细胞凋亡中的作用。最后，综述了年龄对人T细胞中TNF-α诱导的细胞凋亡影响的分子基础。
