Induction of Fas ligand-mediated apoptosis by interferon-α
Induction of Fas ligand-mediated apoptosis by interferon-α
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DOI：
10.1006/clim.2000.4866
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发表时间：
2000-06-01
影响因子：
8.6
通讯作者：
Crow, MK
中科院分区：
文献类型：
--
作者：
Kirou, KA;Vakkalanka, RK;Crow, MK
干扰素-α是最早被研究的细胞因子之一，也是最早用于临床治疗病毒感染和恶性肿瘤的药物。尽管干扰素-α增强NK细胞对病毒感染的靶细胞或肿瘤细胞的杀伤作用已被证实，但其机制尚未完全阐明。在此，我们报道了干扰素-α刺激健康供者的PBMC诱导Fas(CD95)配体(FasL)转录，并导致细胞表面仅在NK细胞部分快速表达。此外，干扰素-α增强了正常PBMC对Fas敏感的淋巴样肿瘤细胞的快速介导的细胞毒作用。在天然免疫的背景下，干扰素-α诱导的FAST可以被视为在存在有害目标的情况下增强NR细胞毒性的一种有效机制，例如病毒感染或转化的细胞。(C)2000年学术出版社。
Interferon-alpha (IFN-alpha) was among the first cytokines studied and the earliest to be used in clinical medicine for the treatment of viral infections and malignancies. Although the capacity of IFN-alpha to augment NK cell cytotoxicity against virus-infected target cells or tumor cells is well established, the mechanism has not been fully elucidated. Here we report that IFN-alpha stimulation of PBMC from healthy donors induces Fas (CD95) ligand (FasL) transcription and leads to increased cell surface Fast expression exclusively on the NK cell fraction. Furthermore, IFN-alpha augments the Fast-mediated cytotoxicity of normal PBMC against Fas-sensitive lymphoid tumor cells. In the context of innate immunity, induction of Fast by IFN-alpha can be viewed as an efficient mechanism to potentiate NR cell cytotoxicity in the presence of harmful targets, such as virally infected or transformed cells. (C) 2000 Academic Press.