He Jeannie Q, Oganesyan Gagik, Saha Supriya K, Zarnegar Brian, Cheng Genhong
Department of Microbiology, Immunology and Molecular Genetics, 8University of California, Los Angeles, Los Angeles, California 90095, USA.
Adv Exp Med Biol. 2007;597:48-59. doi: 10.1007/978-0-387-70630-6_4.
Tumor necrosis factor receptor associated factor 3 (TRAF3) is one of the most enigmatic members in the TRAF family that consists of six members, TRAF1 to 6. Despite its similarities with other TRAFs in terms of structure and protein-protein association, overexpression of TRAF3 does not induce activation of the commonly known TRAF-inducible signaling pathways, namely NF-kappaB and JNK. This lack of a simple functional assay in combination with the mysterious early lethality of the TRAF3-deficient mice has made the study of the biological function of TRAF3 challenging for almost ten years. Excitingly, TRAF3 has been identified recently to perform two seemingly distinct roles. Namely, TRAF3 functions as a negative regulator of the NF-kappaB pathway and separately, as a positive regulator of type I IFN production, placing itself as a critical regulator of both innate and adaptive immune responses.
肿瘤坏死因子受体相关因子3（TRAF3）是TRAF家族中最神秘的成员之一，该家族由TRAF1至TRAF6六个成员组成。尽管TRAF3在结构和蛋白质-蛋白质相互作用方面与其他TRAFs相似，但TRAF3的过表达并不会诱导常见的TRAF诱导信号通路（即核因子κB和JNK）的激活。由于缺乏简单的功能检测方法，再加上TRAF3缺陷小鼠神秘的早期致死性，使得对TRAF3生物学功能的研究在近十年里一直具有挑战性。令人兴奋的是，最近已确定TRAF3发挥两种看似不同的作用。即TRAF3作为核因子κB通路的负调节因子，另外还作为I型干扰素产生的正调节因子，使其成为先天性和适应性免疫反应的关键调节因子。
