在真核生物體內(nèi),，除了能夠識(shí)別入侵機(jī)體的病毒RNA的TOLL樣受體外,，近年來(lái)發(fā)現(xiàn)了另一種能夠識(shí)別病毒RNA的細(xì)胞質(zhì)內(nèi)受體RIG-I,。RIG-I能夠識(shí)別多種RNA 病毒如丙型肝炎病毒（hepatitis C virus,HCV）病毒的雙鏈RNA組分,，并通過(guò)自身的CARD與下游信號(hào)分子MAVS的CARD相互作用來(lái)傳遞信號(hào),，激活細(xì)胞轉(zhuǎn)錄因子IRF-3和NF-κB,，使其進(jìn)入細(xì)胞核內(nèi),，誘導(dǎo)抗病毒干擾素的表達(dá)，從而啟動(dòng)固有免疫應(yīng)答和調(diào)節(jié)隨后的獲得性免疫應(yīng)答,，增強(qiáng)機(jī)體抵抗病毒感染的能力,。
中科院上海生命科學(xué)院/上海交通大學(xué)醫(yī)學(xué)院健康科學(xué)研究所孔玲博士研究生在導(dǎo)師戈寶學(xué)研究員的指導(dǎo)下,，發(fā)現(xiàn)用LPS（一種細(xì)菌感染的主要成份）刺激小鼠外周巨噬細(xì)胞可誘導(dǎo)RIG-I的表達(dá)。在巨噬細(xì)胞和293細(xì)胞中,，RIG-I 和細(xì)胞骨架蛋白Actin相互作用而且共定位,。特異性的siRNA“knock-down”RIG-I 或基因敲除RIG-I降低了巨噬細(xì)胞對(duì)細(xì)菌的吞噬能力。此外,，RIG-I基因剔除小鼠對(duì)細(xì)菌感染較正常小鼠的敏感性明顯增強(qiáng),。這一研究結(jié)果表明RIG-I是寄主抵抗細(xì)菌感染的一個(gè)非常重要的調(diào)控分子。
這項(xiàng)研究工作于2009年8月發(fā)表在《細(xì)胞宿主與微生物》(Cell Host & Microbe)上,，該研究工作得到了國(guó)家自然科學(xué)基金,、科技部973和衛(wèi)生部重大專(zhuān)項(xiàng)的支持。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
