摘要
Detection of pathogen-derived nucleic acids by pattern recognition receptors (PRRs) is essential for the host to mount an appropriate immune response, which for viruses involves the induction of type I interferons (IFNs). By contrast, inappropriate activation of PRRs by self nucleic acids can lead to autoimmunity. Recent developments in PRR research have uncovered important new molecular details as to how Toll-like receptors (TLRs) and retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs) distinguish pathogen from self RNA, while the discovery of cytosolic DNA sensing pathways for IFN induction has revealed completely new innate signaling mechanisms, and also questions how innate immunity discriminates between self and non-self DNA, if at all.
摘要译文
检测的病原体衍生的核酸通过模式识别受体（的PRR）是必不可少的主机安装一个适当的免疫应答，其对于病毒包括I型干扰素（干扰素）的诱导。与此相反，通过的PRR自核酸的不适当的激活可导致自身免疫。在PRR研究最近的发展已经发现重要的新的分子细节，以Toll样如何受体（TLR）和视黄酸可诱导的基因-I（RIG-I）样受体（RLRs）区分自RNA的病原体，而在发现细胞质DNA检测途径诱导干扰素透露全新与生俱来的信令机制，还质疑先天免疫自我和非自DNA之间如何鉴别，如果在所有。
Claudia Gürtler; Andrew G. Bowie. Innate immune detection of microbial nucleic acids[J]. Trends in Microbiology, 2013,21(8): 413–420