Immune response in stat2 knockout mice
Immune response in stat2 knockout mice
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DOI：
10.1016/s1074-7613(00)00077-7
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发表时间：
2000-12-01
期刊：
影响因子：
32.4
通讯作者：
Schindler, C
中科院分区：
文献类型：
--
作者：
Park, C;Li, S;Schindler, C
I型ifn通过Stat1和Stat2诱导基因表达，而Stat1和Stat2又可以结合形成Stat1同型二聚体，或者转录因子ISGF-3 Stat1同型二聚体也可以转导ifn - γ信号。为了探索Stat2和ISGF-3在I型IFN信号传导中的独特特性，我们将其基因靶向删除。Stat2缺失小鼠在免疫应答中表现出许多缺陷。这包括对病毒感染的易感性增加和I型IFN自分泌/旁分泌环的缺失，而这反过来又调节免疫反应的几个方面。有趣的是，stat2缺陷成纤维细胞对I型ifn的反应比巨噬细胞表现出更显著的缺陷，突出了对该配体家族反应的组织特异性差异。
Type I IFNs induce gene expression through Stat1 and Stat2, which can in turn associate either to form Stat1 homodimers or the transcription factor ISGF-3 Stat1 homodimers also transduce signals for IFN-gamma. To explore the unique properties of Stat2 and ISGF-3 in type I IFN signaling, its gene was targeted for deletion. Stat2 null mice exhibit a number of defects in immune response. This includes an increased susceptibility to viral infection and the loss of a type I IFN autocrine/paracrine loop, which in turn regulates several aspects of immune response. Intriguingly, Stat2-deficient fibroblasts exhibit a more significant defect in their response to type I IFNs than macrophages, highlighting tissue-specific differences in the response to this family of ligands.