Zhong Bo, Wang Yan-Yi, Shu Hong-Bing
College of Life Sciences, Wuhan University, Wuhan, 430072 China.
Front Biol (Beijing). 2010;5(1):12-31. doi: 10.1007/s11515-010-0013-x. Epub 2010 Feb 1.
Host pattern recognition receptors (PRRs) recognize invading viral pathogens and initiate a series of signaling cascades that lead to the expression of type I interferons (IFNs) and inflammatory cytokines. During the past decade, significant progresses have been made to characterize PRRs such as Toll-like receptors (TLRs) and RIG-I-like receptors (RLRs) and elucidate the molecular mechanisms of TLR- and RLR-mediated signaling. To avoid excessive and harmful immune effects caused by over-activation of these signaling pathways, host cells adopt a number of strategies to regulate them. In addition, invading viruses also employ a variety of mechanisms to inhibit the production of type I IFNs, thereby evading the supervision and clearance by the host. In this review, we briefly summarize the TLR- and RLR-mediated type I IFN signaling and then focus on the mechanisms by which host cellular and viral components regulate the expression of type I IFNs.
宿主模式识别受体（PRR）识别入侵的病毒病原体，并启动一系列信号级联反应，从而导致I型干扰素（IFN）和炎性细胞因子的表达。在过去十年中，在表征诸如Toll样受体（TLR）和RIG-I样受体（RLR）等PRR以及阐明TLR和RLR介导的信号传导的分子机制方面取得了重大进展。为避免这些信号通路过度激活引起的过度和有害免疫效应，宿主细胞采用多种策略对其进行调节。此外，入侵病毒也采用多种机制抑制I型IFN的产生，从而逃避宿主的监测和清除。在本综述中，我们简要总结了TLR和RLR介导的I型IFN信号传导，然后重点关注宿主细胞成分和病毒成分调节I型IFN表达的机制。
