ID2 inhibits innate antiviral immunity by blocking TBK1- and IKKε-induced activation of IRF3

作者：Congci Yu, Bei Wang, Yue Zhu, Chongyang Zhang, Lili Ren, Xiaobo Lei, Zichun Xiang, Zhuo Zhou, He Huang, Jianwei Wang, Zhendong Zhao · 发表于：Science Signaling · 年份：2022 · DOI：10.1126/scisignal.abh0068 · 被引用次数：12 · 研究领域：interferon and immune responses、Immune Cell Function and Interaction、NF-κB Signaling Pathways

). IFN-β induced the nuclear export of ID2 to form a negative feedback loop. Knocking out ID2 in human cells enhanced innate immune responses and suppressed infection by different viruses, including SARS-CoV-2. Mice with a myeloid-specific deficiency of ID2 produced more IFN-α in response to viral infection and were more resistant to viral infection than wild-type mice. Our findings not only establish ID2 as a modulator of IRF3 activation induced by TBK1 and/or IKKε but also introduce a mechanism for cross-talk between innate immunity and cell development and differentiation.