Characterization of the interferon regulatory factor 3-mediated antiviral response in a cell line deficient for IFN production
Characterization of the interferon regulatory factor 3-mediated antiviral response in a cell line deficient for IFN production
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DOI：
10.1016/j.molimm.2008.10.010
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发表时间：
2009-01-01
影响因子：
3.6
通讯作者：
Mossman, Karen L.
中科院分区：
文献类型：
--
作者：
Chew, Tracy;Noyce, Ryan;Mossman, Karen L.
病毒颗粒进入非免疫细胞的先天细胞应答需要干扰素调节因子3 （IRF-3）的转录活性，而不是I型干扰素（IFN）的产生。在这里，我们描述了猴肾上皮细胞系Vero细胞对病毒源性刺激的IFN非依赖性先天细胞反应，这是一种缺乏IFN产生的猴肾上皮细胞系。我们提供的证据表明，Vero细胞缺乏对传入的病毒颗粒或多肌苷：多胞苷酸（pIC）（一种dsRNA模拟物）进行依赖irf -3、不依赖ifn的抗病毒应答的能力。我们进一步证明，IRF-3蛋白的丰度是pic介导的抗病毒信号通路的决定因素。这些观察结果进一步表征了Vero细胞对病毒感染的宽容性质，并强调了IRF-3在先天抗病毒反应中的重要参与。(C) 2008 Elsevier Ltd版权所有。
The innate cellular-response to virus particle entry in non-immune cells requires the transcriptional activity of interferon regulatory factor 3 (IRF-3), but not production of type I interferon (IFN). Here, we characterize the IFN-independent innate cellular response to virus-derived stimuli in Vero cells, a monkey kidney epithelial cell line deficient for IFN production. We provide evidence that Vero cells are deficient in their ability to mount an IRF-3-dependent, IFN-independent antiviral response against either incoming Virus particles or polyinosinic:polycytidylic acid (pIC), a dsRNA mimetic. We further demonstrate that abundance of IRF-3 protein is a determinant in the pIC-mediated antiviral signalling pathway. These observations further characterize the permissive nature of Vero cells to viral infection, and highlight the Crucial involvement of IRF-3 in the innate antiviral response. (C) 2008 Elsevier Ltd. All rights reserved.