Laboratory of Host Defense, WPI Immunology Frontier Research Center, Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Immunol Rev. 2011 Sep;243(1):61-73. doi: 10.1111/j.1600-065X.2011.01048.x.
Host cells trigger signals for innate immune responses upon recognition of conserved structures in microbial pathogens. Nucleic acids, which are critical components for inheriting genetic information in all species including pathogens, are key structures sensed by the innate immune system. The corresponding receptors for foreign nucleic acids include members of Toll-like receptors, RIG-I-like receptors, and intracellular DNA sensors. While nucleic acid recognition by these receptors is required for host defense against the pathogen, there is a potential risk to the host of self-nucleic acids recognition, thus precipitating autoimmune and autoinflammatory diseases. In this review, we discuss the roles of nucleic acid-sensing receptors in guarding against pathogen invasion, discriminating between self and non-self, and contributing to autoimmunity and autoinflammatory diseases.
宿主细胞在识别微生物病原体中保守结构时，会触发先天免疫反应信号。核酸是包括病原体在内的所有物种遗传信息的关键组成部分，是先天免疫系统感知的关键结构。识别外来核酸的相应受体包括 Toll 样受体、RIG-I 样受体和细胞内 DNA 传感器的成员。虽然这些受体识别核酸是宿主抵抗病原体的防御所必需的，但宿主自身核酸的识别存在潜在风险，从而引发自身免疫和自身炎症性疾病。在这篇综述中，我们讨论了核酸感应受体在抵御病原体入侵、区分自我和非自我以及导致自身免疫和自身炎症性疾病方面的作用。
