Kawai Taro, Akira Shizuo
Laboratory of Host Defense, Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Ann N Y Acad Sci. 2008 Nov;1143:1-20. doi: 10.1196/annals.1443.020.
Toll-like receptors (TLRs) and RIG-I-like receptors (RLRs) constitute distinct families of pattern-recognition receptors that sense nucleic acids derived from viruses and trigger antiviral innate immune responses. TLR3, TLR7, and TLR9 are membrane proteins localized to the endosome that recognize viral double-stranded RNA, single-stranded RNA, and DNA, respectively, while RLRs, including RIG-I, Mda5, and LGP2, are cytoplasmic proteins that recognize viral RNA. Upon recognition of these nucleic acid species, TLRs and RLRs recruit specific intracellular adaptor proteins to initiate signaling pathways culminating in activation of NF-kappaB, MAP kinases, and IRFs that control the transcription of genes encoding type I interferon and other inflammatory cytokines, which are important for eliminating viruses. Here, we review recent insights into the signaling pathways initiated by TLR and RLR and their roles in innate and adaptive immune responses.
Toll样受体（TLR）和维甲酸诱导基因I样受体（RLR）构成了不同的模式识别受体家族，它们能够识别源自病毒的核酸并触发抗病毒先天性免疫反应。TLR3、TLR7和TLR9是定位于内涵体的膜蛋白，分别识别病毒双链RNA、单链RNA和DNA，而包括维甲酸诱导基因I（RIG-I）、黑色素瘤分化相关基因5（Mda5）和实验室遗传学与生理学2（LGP2）在内的RLR是识别病毒RNA的细胞质蛋白。在识别这些核酸种类后，TLR和RLR招募特定的细胞内衔接蛋白来启动信号通路，最终激活核因子κB（NF-κB）、丝裂原活化蛋白激酶（MAP激酶）和干扰素调节因子（IRF），这些因子控制着编码I型干扰素和其他炎性细胞因子的基因的转录，这对于清除病毒很重要。在此，我们综述了关于由TLR和RLR启动的信号通路及其在先天性和适应性免疫反应中的作用的最新见解。
