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J Zhejiang Univ (Med Sci)  2017, Vol. 46 Issue (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
HE Yujie1,2(),PAN Jianping1,*()
1. School of Medicine, Zhejiang University City College, Hangzhou 310015, China
2. Department of Medical Microbiology and Parasitology, Zhejiang University School of Medicine, Hangzhou 310058, China
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Abstract  

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.



Key wordsBacteria      Immunity, natural      Toll-like receptors/immunology      Membrane glycoproteins/immunology      Signal transduction      Receptors, pattern recognition      Receptors, cell surface      Review     
Received: 02 December 2016      Published: 07 August 2017
Corresponding Authors: PAN Jianping     E-mail: 21418015@zju.edu.cn;jppan@zucc.edu.cn
Cite this article:

HE Yujie,PAN Jianping. Progress on mechanisms for pathogensto evade NOD-like receptor and Toll-like receptor signaling pathways. J Zhejiang Univ (Med Sci), 2017, 46(2): 218-224.

URL:

http://www.zjujournals.com/xueshu/med/10.3785/j.issn.1008-9292.2017.04.16     OR     http://www.zjujournals.com/xueshu/med/Y2017/V46/I2/218


病原菌对NOD样受体及Toll样受体信号通路介导的固有免疫逃逸机制研究进展

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。


关键词: 细菌,  免疫,天然,  Toll样受体/免疫学,  膜糖蛋白类/免疫学,  信号转导,  受体,模式识别,  受体,细胞表面,  综述 
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