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. 2017 Mar 25;46(2):218-224.
doi: 10.3785/j.issn.1008-9292.2017.04.16.

[Progress on mechanisms for pathogensto evade NOD-like receptor and Toll-like receptor signaling pathways]

[Article in Chinese]
H E Yujie  1 , Pan Jianping  2
Affiliations

[Progress on mechanisms for pathogensto evade NOD-like receptor and Toll-like receptor signaling pathways]

[Article in Chinese]
H E Yujie et al. Zhejiang Da Xue Xue Bao Yi Xue Ban. .

Abstract
in English, Chinese

The innate immune system provides a first line of defense against invading pathogens, in which the pattern recognition receptors (PRR) recognize pathogen-associated molecular patterns (PAMP) and initiate the downstream signaling pathways to eliminate the encountered pathogens. There are two main classes of such signaling pathways: NOD-like receptor (NLR) signaling pathway and Toll-like receptor (TLR) signaling pathway. The microbial pathogens under selective pressure have evolved numerous mechanisms to avoid and/or manipulate the NLR and TLR signal transduction for survival and replication. To evade the NLR signaling pathway, pathogens interfere and/or inhibit inflammasome activation in innate immune cells by producing virulence factors or reducing PAMPs expression. The mechanisms for pathogens to evade TLR signaling pathway include: inhibition of mitogen activated protein kinases (MAPKs) cascade reaction, inhibition of NF-КB activation, and interference of down-stream signal transduction by producing Toll/interleukin-1 receptor (TIR)-containing proteins which bind directly with TLRs or adaptor proteins in the signaling pathway.

作为机体抵抗病原微生物的第一道防线，固有免疫细胞通过模式识别受体（PRR）识别病原体相关模式分子（PAMP）继而启动下游信号通路，以发挥固有免疫效应，清除入侵的病原体和异物。固有免疫细胞主要的信号通路有NOD样受体（NLR）及Toll样受体（TLR）信号通路，病原菌经过长期的选择进化产生了针对NLR及TLR信号通路的对抗机制，以利于其在宿主体内的生存增殖。病原菌主要通过产生毒力因子或降低刺激炎症小体活化的PAMP的表达，干扰、抑制或避免固有免疫细胞内炎症小体的活化，实现对NLR介导的信号通路的免疫逃逸。而对TLR信号通路的免疫逃逸主要通过产生毒力因子，抑制丝裂原活化蛋白激酶级联反应、抑制NF-κB活化以及通过产生含有TIR结构域的蛋白，直接与TLR或者TLR信号通路中的接头蛋白结合，干扰下游信号转导三种机制。

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