Interferon-stimulated gene 60 (ISG60) constitutes a negative feedback loop in the downstream of TLR3 signaling in hCMEC/D3 cells
Interferon-stimulated gene 60 (ISG60) constitutes a negative feedback loop in the downstream of TLR3 signaling in hCMEC/D3 cells
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DOI：
10.1016/j.jneuroim.2018.08.016
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发表时间：
2018-11-15
影响因子：
3.3
通讯作者：
Tanaka, Hiroshi
中科院分区：
文献类型：
--
作者：
Imaizumi, Tadaatsu;Sassa, Naoko;Tanaka, Hiroshi
脑毛细血管内皮细胞是血脑屏障的组成部分，是抵御病毒侵入大脑的第一道防线。我们证明，用 Toll 样受体 3 (TLR3) 激动剂聚肌苷-聚胞苷酸 (poly IC) 处理 hCMEC/D3 细胞（一种人脑毛细血管内皮细胞系）可诱导干扰素 (IFN) 刺激的基因 60 (ISG60) 的表达，并且该反应是由 IFN-β 介导的。 ISG60 的敲低增加了聚 IC 诱导的 IFN-β 和 IFN-β 诱导趋化因子 CXCL10 的表达。这表明ISG60在TLR3/IFN-β下游构成负反馈环。脑毛细血管内皮细胞中的 ISG60 可能有助于防止与病毒感染相关的过度免疫反应。
Brain capillary endothelial cells are the component of blood brain barrier, and the first line of defense against viruses invading into brain. We demonstrate that treatment of hCMEC/D3 cells, a human brain capillary endothelial cell line, with a Toll-like receptor 3 (TLR3) agonist polyinosinic-polycytidylic acid (poly IC) induces the expression of interferon (IFN)-stimulated gene 60 (ISG60), and this reaction was mediated by IFN-beta. Knockdown of ISG60 increased the poly IC-induced expression of IFN-beta and an IFN-beta-inducible chemokine CXCL10. This indicates that ISG60 constitutes a negative feedback loop in the downstream of TLR3/IFN-beta. ISG60 in brain capillary endothelial cells may contribute to prevent excess immune reactions associated with viral infections.