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Activation of STAT6 by STING Is Critical for Antiviral Innate Immunity

lele 添加于 2011-10-24 18:38 | 2261 次阅读 | 0 个评论

作者
Chen H, Sun H, You F, Sun W, Zhou X, Chen L, Yang J, Wang Y, Tang H, Guan Y, Xia W, Gu J, Ishikawa H, Gutman D, Barber G, Qin Z, Jiang Z
摘要
STAT6 plays a prominent role in adaptive immunity by transducing signals from extracellular cytokines. We now show that STAT6 is required for innate immune signaling in response to virus infection. Viruses or cytoplasmic nucleic acids trigger STING (also named MITA/ERIS) to recruit STAT6 to the endoplasmic reticulum, leading to STAT6 phosphorylation on Ser⁴⁰⁷ by TBK1 and Tyr⁶⁴¹, independent of JAKs. Phosphorylated STAT6 then dimerizes and translocates to the nucleus to induce specific target genes responsible for immune cell homing. Virus-induced STAT6 activation is detected in all cell-types tested, in contrast to the cell-type specific role of STAT6 in cytokine signaling, and Stat6^/ mice are susceptible to virus infection. Thus, STAT6 mediates immune signaling in response to both cytokines at the plasma membrane, and virus infection at the endoplasmic reticulum.
详细资料
- 文献种类:期刊
- 期刊名称: Cell
- 期刊缩写: Cell
- 期卷页: 2011年第147卷第2期 436-446页
- ISBN: 0092-8674
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附件
Activation of STAT6 by STING Is Critical for Antiviral Innate Immunity
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