Graduate School of Pharmaceutical Sciences, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
Curr Opin Struct Biol. 2017 Dec;47:52-59. doi: 10.1016/j.sbi.2017.05.010. Epub 2017 Jun 7.
Toll-like receptors (TLRs) activate the innate immune system in response to invading pathogens. Although nucleic acids are one of the principal TLR ligands, they are not inherently pathogen-specific and, thus, carry the risk of triggering autoimmunity. There are multiple unique regulatory mechanisms aimed at preventing accidental activation of nucleic acid-sensing TLRs. Recent structural studies revealed that different nucleic acid-sensing TLRs have specific modes of recognizing nucleic acids as ligands regulated by diverse regulation mechanism both at the receptor and ligand levels. This review summarizes structural knowledge on the ligand recognition and regulation mechanism by nucleic acid-sensing TLRs.
Toll 样受体（TLRs）可识别病原体相关分子模式，激活固有免疫。核酸是 TLR 配体之一，但核酸不具有病原体的特异性，可诱发自身免疫。因此，机体会通过多种机制来避免核酸被 TLR 识别。近期结构生物学研究揭示，不同 TLR 通过不同的调控机制识别不同的核酸模式，这种特异性主要取决于 TLR 与核酸结合的结构特征。本文就核酸识别的 TLR 结构特征及其调控机制进行综述。
