Effector-triggered immunity and pathogen sensing in metazoans.
Effector-triggered immunity and pathogen sensing in metazoans.
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DOI：
10.1038/s41564-019-0623-2
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发表时间：
2020-01
影响因子：
28.3
通讯作者：
中科院分区：
文献类型：
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作者：
微生物病原体拥有一系列策略来入侵宿主，逃避免疫防御和促进感染。特别是，细菌使用毒力因子，如分泌的毒素和效应蛋白，操纵宿主细胞过程并建立复制生态位。真核生物在面对这种挑战时的生存需要宿主机制来检测和抵消这些病原体特异性毒力策略。在这篇综述中，我们专注于效应触发免疫（ETI）在后生动物生物体作为一种机制，病原体的传感和区分病原微生物从非病原微生物。为了这次审查的目的，我们采用的概念ETI制定最初的背景下，植物病原体及其宿主，其中特定的宿主蛋白质“守卫”中央细胞过程，并触发炎症反应后，病原体驱动的中断这些过程。虽然ETI的分子机制在植物中得到了很好的描述，但我们对后生动物中功能类似机制的理解仍然是新兴的。在这篇综述中，我们提出了一个概述，ETI在后生动物和讨论最近描述的细胞过程，由主机守卫。虽然所有的病原体操纵宿主途径，我们主要集中在细菌病原体，并强调效应触发的免疫防御的途径，感测病原体的核心细胞过程的中断。最后，我们讨论了最近的事态发展，我们的理解病原体如何逃避ETI克服这些主机的适应。
Microbial pathogens possess an arsenal of strategies to invade their hosts, evade immune defences and promote infection. In particular, bacteria use virulence factors, such as secreted toxins and effector proteins, to manipulate host cellular processes and establish a replicative niche. Survival of eukaryotic organisms in the face of such challenge requires host mechanisms to detect and counteract these pathogen-specific virulence strategies. In this Review, we focus on effector-triggered immunity (ETI) in metazoan organisms as a mechanism for pathogen sensing and distinguishing pathogenic from non-pathogenic microorganisms. For the purposes of this Review, we adopt the concept of ETI formulated originally in the context of plant pathogens and their hosts, wherein specific host proteins ‘guard’ central cellular processes and trigger inflammatory responses following pathogen-driven disruption of these processes. While molecular mechanisms of ETI are well-described in plants, our understanding of functionally analogous mechanisms in metazoans is still emerging. In this Review, we present an overview of ETI in metazoans and discuss recently described cellular processes that are guarded by the host. Although all pathogens manipulate host pathways, we focus primarily on bacterial pathogens and highlight pathways of effector-triggered immune defence that sense disruption of core cellular processes by pathogens. Finally, we discuss recent developments in our understanding of how pathogens can evade ETI to overcome these host adaptations.
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影响因子：
6.7
作者：
Bruno VM;Hannemann S;Lara-Tejero M;Flavell RA;Kleinstein SH;Galán JE
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Sander, Leif E.
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Staskawicz, BJ
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