在真核生物体内，除了能够识别入侵机体的病毒RNA的TOLL样受体外，近年来发现了另一种能够识别病毒RNA的细胞质内受体RIG-I。RIG-I能够识别多种RNA 病毒如丙型肝炎病毒（hepatitis C virus,HCV）病毒的双链RNA组分，并通过自身的CARD与下游信号分子MAVS的CARD相互作用来传递信号，激活细胞转录因子IRF-3和NF-κB，使其进入细胞核内，诱导抗病毒干扰素的表达，从而启动固有免疫应答和调节随后的获得性免疫应答，增强机体抵抗病毒感染的能力。
中科院上海生命科学院/上海交通大学医学院健康科学研究所孔玲博士研究生在导师戈宝学研究员的指导下，发现用LPS（一种细菌感染的主要成份）刺激小鼠外周巨噬细胞可诱导RIG-I的表达。在巨噬细胞和293细胞中，RIG-I 和细胞骨架蛋白Actin相互作用而且共定位。特异性的siRNA“knock-down”RIG-I 或基因敲除RIG-I降低了巨噬细胞对细菌的吞噬能力。此外，RIG-I基因剔除小鼠对细菌感染较正常小鼠的敏感性明显增强。这一研究结果表明RIG-I是寄主抵抗细菌感染的一个非常重要的调控分子。
这项研究工作于2009年8月发表在《细胞宿主与微生物》(Cell Host & Microbe)上，该研究工作得到了国家自然科学基金、科技部973和卫生部重大专项的支持。（生物谷Bioon.com）
生物谷推荐原始出处：
Cell Host & Microbe,20 August 2009 doi:10.1016/j.chom.2009.06.008
An Essential Role for RIG-I in Toll-like Receptor-Stimulated Phagocytosis
Ling Kong1,4,6,Lei Sun1,4,6,Hongxin Zhang2,Qin Liu1,Ye Liu1,Linhua Qin1,Guojun Shi1,4,Jun-Hao Hu1,4,Ajing Xu1,Yue-Ping Sun2,Dangsheng Li5,Yu-Fang Shi1,Jing-Wu Zang1,Jiang Zhu3,Zhu Chen3,Zhu-Gang Wang2,3,,andBao-Xue Ge1,,
1 The Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai JiaoTong University School of Medicine, Shanghai 200025, China
2 Laboratory of Genetic Engineering, Department of Medical Genetics, Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, China
3 State Key Laboratory for Medical Genomics and Shanghai Institute of Hematology, RuiJin Hospital, Shanghai 200025, China
4 Graduate School of Chinese Academy of Sciences, Beijing 100039, China
5 Shanghai Information Center for Life Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China
Retinoic acid-inducible gene-I (RIG-I) plays an important role in antiviral response by recognizing double-stranded RNA. Here we demonstrate an unanticipated role of RIG-I in Toll-like receptor (TLR)-stimulated phagocytosis. Stimulation with lipopolysaccharide (LPS), a ligand of TLR4, induced the expression of RIG-I in macrophages. Depletion of RIG-I by RNAi or gene targeting inhibited the LPS-induced phagocytosis of bacteria. Cellular processes involved in phagocytosis, such as small GTPase Cdc42/Rac1 activation, actin polymerization, and actin-regulator Arp2/3 recruitment, were also impaired in RIG-I-deficient macrophages activated by LPS. Moreover, RIG-I/ mice were found to be more susceptible to infection with Escherichia coli as compared to wild-type mice. Thus, the regulatory functions of RIG-I are strikingly broad, including a role not only in antiviral responses but in antibacterial responses as well.
