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病原体用于逃避凝集素补体途径的机制。

Evasion Mechanisms Used by Pathogens to Escape the Lectin Complement Pathway.

作者信息

Rosbjerg Anne, Genster Ninette, Pilely Katrine, Garred Peter

机构信息

Laboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, Rigshospitalet, Faculty of Health and Medical Sciences, University of CopenhagenCopenhagen, Denmark.

出版信息

Front Microbiol. 2017 May 12;8:868. doi: 10.3389/fmicb.2017.00868. eCollection 2017.

DOI:10.3389/fmicb.2017.00868
PMID:28553281
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5427104/
Abstract

The complement system is a crucial defensive network that protects the host against invading pathogens. It is part of the innate immune system and can be initiated via three pathways: the lectin, classical and alternative activation pathway. Overall the network compiles a group of recognition molecules that bind specific patterns on microbial surfaces, a group of associated proteases that initiates the complement cascade, and a group of proteins that interact in proteolytic complexes or the terminal pore-forming complex. In addition, various regulatory proteins are important for controlling the level of activity. The result is a pro-inflammatory response meant to combat foreign microbes. Microbial elimination is, however, not a straight forward procedure; pathogens have adapted to their environment by evolving a collection of evasion mechanisms that circumvent the human complement system. Complement evasion strategies features different ways of exploiting human complement proteins and moreover features different pathogen-derived proteins that interfere with the normal processes. Accumulated, these mechanisms target all three complement activation pathways as well as the final common part of the cascade. This review will cover the currently known lectin pathway evasion mechanisms and give examples of pathogens that operate these to increase their chance of invasion, survival and dissemination.

摘要

补体系统是一个关键的防御网络,可保护宿主抵御入侵的病原体。它是固有免疫系统的一部分,可通过三条途径启动:凝集素途径、经典途径和替代激活途径。总体而言,该网络由一组结合微生物表面特定模式的识别分子、一组启动补体级联反应的相关蛋白酶以及一组在蛋白水解复合物或末端孔形成复合物中相互作用的蛋白质组成。此外,各种调节蛋白对于控制活性水平很重要。其结果是产生一种旨在对抗外来微生物的促炎反应。然而,微生物的清除并非一个简单的过程;病原体通过进化出一系列规避人类补体系统的逃避机制来适应其环境。补体逃避策略具有利用人类补体蛋白的不同方式,而且还具有干扰正常过程的不同病原体衍生蛋白。这些机制累积起来会针对所有三条补体激活途径以及级联反应的最终共同部分。本综述将涵盖目前已知的凝集素途径逃避机制,并举例说明利用这些机制来增加其入侵、存活和传播机会的病原体。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8d1/5427104/753278b7515e/fmicb-08-00868-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8d1/5427104/753278b7515e/fmicb-08-00868-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8d1/5427104/753278b7515e/fmicb-08-00868-g001.jpg

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Association of Mannose-binding Lectin Polymorphisms with Tuberculosis Susceptibility among Chinese.甘露聚糖结合凝集素基因多态性与中国人结核病易感性的关系
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Secreted NS1 Protects Dengue Virus from Mannose-Binding Lectin-Mediated Neutralization.分泌型NS1蛋白可保护登革病毒免受甘露糖结合凝集素介导的中和作用。
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Host Immune Responses to Salivary Components - A Critical Facet of Tick-Host Interactions.宿主对唾液成分的免疫反应——蜱-宿主相互作用的关键方面。
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