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首页> 外文期刊>Cytokine >IFNalpha regulates NK cell cytotoxicity through STAT1 pathway.
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IFNalpha regulates NK cell cytotoxicity through STAT1 pathway.

机译：IFNalpha通过STAT1途径调节NK细胞的细胞毒性。

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Human natural killer (NK) cell lines (YT and NK-92) and freshly isolated human NK cells were used to determine signal pathway (s) and their cytolysis-related molecules involved in IFNalpha-stimulated natural cytotoxicity. NK cells displayed apparently augmented cytotoxicity against target tumor cells (K562) and up-regulated gene expression of cytolytic effectors Fas-L and perforin in response to IFNalpha stimulation. Meanwhile, the tyrosine phosphorylation of STAT1 of NK cells was quickly induced, but other pathways including STAT3, STAT6, ERK1/2, p38 MAPK, JNK/SAPK, PI-3K, NF-kappaB were not or only weakly activated. Transient expression of dominant-negative form of STAT1 (DN STAT1) markedly inhibited STAT1 activation and then alleviated cytolysis activity of IFNalpha-treated YT cells, which was correlated to a markedly down-regulated expression of IRF-1, a key transcription factor necessary for cytotoxicity of IFNalpha/beta-activated NK cells. The results indicate that STAT1 activation play a crucialrole in IFNalpha signaling for cytolysis function of NK cells.
机译：人类自然杀伤（NK）细胞系（YT和NK-92）和新鲜分离的人类NK细胞用于确定信号通路及其参与IFNα刺激的自然细胞毒性的细胞溶解相关分子。 NK细胞表现出明显增强的针对靶肿瘤细胞（K562）的细胞毒性，并响应IFNα刺激而使溶细胞效应因子Fas-L和穿孔素的基因表达上调。同时，NK细胞STAT1的酪氨酸磷酸化很快被诱导，但是其他途径包括STAT3，STAT6，ERK1 / 2，p38 MAPK，JNK / SAPK，PI-3K，NF-κB未被激活或仅被弱激活。 STAT1（DN STAT1）显性负型的瞬时表达显着抑制STAT1激活，然后减轻IFNalpha处理的YT细胞的细胞溶解活性，这与IRF-1的表达明显下调相关，IRF-1是必需的关键转录因子IFNα/β激活的NK细胞的细胞毒性。结果表明STAT1激活在NK细胞的细胞溶解功能的IFNalpha信号传导中起着至关重要的作用。

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