School of Life Sciences, Peking University, Beijing, China.
Protein Cell. 2013 Jan;4(1):27-39. doi: 10.1007/s13238-012-2063-0. Epub 2012 Sep 21.
Microbial components and the endogenous molecules released from damaged cells can stimulate germ-line-encoded pattern recognition receptors (PRRs) to transduce signals to the hub of the innate immune signaling network-the adaptor proteins MyD88/TRIF/MAVS/STING/Caspase-1, where integrated signals relay to the relevant transcription factors IRF3/IRF7/NF-κB/ AP-1 and the signal transducer and activator of transcription 6 (STAT6) to trigger the expression of type I interferons and inflammatory cytokines or the assembly of inflammasomes. Most pleiotropic cytokines are secreted and bind to specific receptors, activating the signaling pathways including JAK-STAT for the proliferation, differentiation and functional capacity of immune cells. This review focuses on several critical adaptors in innate immune signaling cascades and recent progress in their molecular mechanisms.
微生物成分和受损细胞释放的内源性分子可以刺激种系编码的模式识别受体 (PRRs) 将信号转导至先天免疫信号网络的枢纽——衔接蛋白 MyD88/TRIF/MAVS/STING/Caspase-1,其中整合信号传递到相关转录因子 IRF3/IRF7/NF-κB/AP-1 和信号转导和转录激活因子 6 (STAT6),以触发 I 型干扰素和炎症细胞因子的表达或炎性小体的组装。大多数多效细胞因子被分泌并与特定受体结合,激活信号通路,包括 JAK-STAT,以促进免疫细胞的增殖、分化和功能能力。本文综述了先天免疫信号级联中的几个关键衔接蛋白及其分子机制的最新进展。