Editorial overview: Attrition warfare: host cell weapons against intracellular pathogens, and how the pathogens fight back.

Editorial overview: Attrition warfare: host cell weapons against intracellular pathogens, and how the pathogens fight back.
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编辑概述:消耗战:针对细胞内病原体的宿主细胞武器,以及病原体如何反击。

DOI:
10.1016/j.coi.2019.07.009
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发表时间:
2019
影响因子:
7
通讯作者:
Glickman,MichaelS
Glickman,MichaelS
中科院分区:
医学2区
文献类型:
--
作者:
Stallings,ChristinaL;Glickman,MichaelS

文献摘要

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细胞内病原体对宿主来说是一个特殊的挑战。由于它们存在于宿主细胞内,消除感染不可避免地需要在最大限度地破坏病原体和最大限度地减少宿主细胞损伤之间取得平衡。病原体破坏和宿主细胞保存之间的这种平衡涉及一系列宿主策略,从直接杀死病原体并保持宿主细胞存活到更具自杀性的策略(牺牲受感染的宿主细胞以促进病原体杀死)。细胞内病原体已经进化来改变这些宿主策略以实现发病机制,从而导致宿主和病原体防御的军备竞赛。在本期中,我们将探讨用于控制细胞内病原体的细胞内在和细胞外在机制的多样性,特别是细菌病原体,以及病原体抵消这些策略的机制。Brewer、Brubaker、Monack [1] 回顾了炎症小体的广泛作用,以及中和炎症小体的病原体对策,在宿主防御中。他们提出了一个概念框架,通过概述不同的传感器、适配器和效应蛋白组装成炎性体复合物,最终导致 pro-IL1B、pro-IL-18 和 Gasdermin D 的裂解,来理解各种炎性体。全面总结了中和这种有效宿主防御机制的多种病原体策略。
Intracellular pathogens represent a special challenge for the host. Because they reside within the host cell, elimination of the infection inevitably involves a balance between maximizing pathogen destruction while minimizing host cell damage. This balance between pathogen destruction and host cell preservation involves a spectrum of host strategies that range from direct pathogen killing with host cell survival to more suicidal strategies in which the infected host cell is sacrificed to facilitate pathogen killing. Intracellular pathogens have evolved to modify these host strategies to enable pathogenesis, leading to an arms race of host and pathogen defenses. In this issue, we will explore the diversity of cell intrinsic and cell extrinsic mechanisms deployed to control intracellular pathogens, with a particular emphasis on bacterial pathogens, and the mechanisms by which pathogens counteract these strategies.Brewer, Brubaker, Monack [1] review the broad role of the inflammasome, and the pathogen countermeasures that neutralize the inflammasome, in host defense. They present a conceptual framework to understand the varied inflammasomes by outlining the distinct sensors, adaptors, and effector proteins that assemble into inflammasome complexes, ultimately leading to cleavage or pro-IL1B, pro-IL-18, and Gasdermin D. The diverse pathogen strategies for neutralizing this potent host defense mechanism are comprehensively summarized.