Innate immunity to nucleic acids forms the backbone for anti-viral immunity and several inflammatory diseases.?

對(duì)核酸先天免疫構(gòu)成了抗病毒免疫和幾種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).?

在檢測(cè)到細(xì)胞質(zhì)中病毒RNA時(shí)，維甲酸誘導(dǎo)的基因-I樣受體（RLRs）與線粒體抗病毒信號(hào)蛋白相互作用，激活TANK結(jié)合激酶1(TBK1)以誘導(dǎo)I型干擾素

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細(xì)胞和B細(xì)胞的發(fā)育過(guò)程中的關(guān)鍵蛋白。該蛋白也表達(dá)于隨喜細(xì)胞中，但是作用不清楚。我們證實(shí)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.