Innate immunity to nucleic acids forms the backbone for anti-viral immunity and several inflammatory diseases.
对核酸先天免疫构成了抗病毒免疫和几种炎性疾病的主要原因
Upon sensing cytosolic viral RNA, retinoic acid-inducible gene-I-like receptors (RLRs) interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1 (TBK1) to induce type I interferon (IFN-I).
在检测到细胞质中病毒RNA时，维甲酸诱导的基因-I样受体（RLRs）与线粒体抗病毒信号蛋白相互作用，激活TANK结合激酶1(TBK1)以诱导I型干扰素
TRAF3-interacting protein 3 (TRAF3IP3, T3JAM) is essential for T and B cell development. It is also wellexpressed by myeloid cells, where its role is unknown. Here we report that TRAF3IP3 suppresses cytosolic poly(I:C), 5’ppp-dsRNA, and vesicular stomatitis virus (VSV) triggers IFN-I expression in overexpression systems and Traf3ip3−/− primary myeloid cells.
TRAF-3相互作用蛋白3是T细胞和B细胞的发育过程中的关键蛋白。该蛋白也表达于随喜细胞中，但是作用不清楚。我们证实了T3JAM抑制
The mechanism of action is through the interaction of TRAF3IP3 with endogenous TRAF3 and TBK1. This leads to the degradative K48 ubiquitination of TBK1 via its K372 residue in a DTX4-dependent fashion.
Mice with myeloid-specific gene deletion of Traf3ip3 have increased RNA virus-triggered IFN-I production and reduced susceptibility to virus. These results identify a function of TRAF3IP3 in the regulation of the host response to cytosolic viral RNA in myeloid cells.
