Laboratory of Molecular Immunobiology, Division of Biological Science, Graduate School of Science and Technology, Nara Institute of Science and Technology (NAIST), Ikoma, Japan.
Front Immunol. 2021 Jan 28;11:625833. doi: 10.3389/fimmu.2020.625833. eCollection 2020.
Recognition of pathogen-derived nucleic acids by pattern-recognition receptors (PRRs) is essential for eliciting antiviral immune responses by inducing the production of type I interferons (IFNs) and proinflammatory cytokines. Such responses are a prerequisite for mounting innate and pathogen-specific adaptive immune responses. However, host cells also use nucleic acids as carriers of genetic information, and the aberrant recognition of self-nucleic acids by PRRs is associated with the onset of autoimmune or autoinflammatory diseases. In this review, we describe the mechanisms of nucleic acid sensing by PRRs, including Toll-like receptors, RIG-I-like receptors, and DNA sensor molecules, and their signaling pathways as well as the disorders caused by uncontrolled or unnecessary activation of these PRRs.
模式识别受体(PRRs)识别病原体衍生的核酸对于通过诱导 I 型干扰素(IFNs)和促炎细胞因子的产生来引发抗病毒免疫反应至关重要。这种反应是引发先天和病原体特异性适应性免疫反应的前提。然而,宿主细胞也将核酸用作遗传信息的载体,并且 PRRs 对自身核酸的异常识别与自身免疫或自身炎症性疾病的发生有关。在这篇综述中,我们描述了 PRRs 识别核酸的机制,包括 Toll 样受体、RIG-I 样受体和 DNA 传感器分子,以及它们的信号通路,以及这些 PRRs 不受控制或不必要激活所导致的疾病。