Molecular mechanisms and functions of pyroptosis, inflammatory caspases and inflammasomes in infectious diseases.
Molecular mechanisms and functions of pyroptosis, inflammatory caspases and inflammasomes in infectious diseases.
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DOI：
10.1111/imr.12534
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发表时间：
2017-05
影响因子：
8.7
通讯作者：
Kanneganti TD
中科院分区：
文献类型：
--
作者：
Man SM;Karki R;Kanneganti TD
细胞死亡是一种基本的生物学现象，对生物体的生存和发展至关重要。新出现的证据也表明，细胞死亡有助于对传染病的免疫防御。焦亡是由人和小鼠半胱天冬酶-1、人半胱天冬酶-4和半胱天冬酶-5或小鼠半胱天冬酶-11激活的炎性程序性细胞死亡途径的形式。这些炎性半胱天冬酶被宿主用来控制细菌、病毒、真菌或原生动物病原体。焦亡需要通过炎性半胱天冬酶裂解和激活成孔效应蛋白gasdermin D。细胞的物理破裂导致促炎细胞因子IL-1β和IL-18、alarmin和内源性炎症相关分子模式的释放，表明焦亡的炎症潜力。在这里，我们描述了炎症性半胱天冬酶和焦亡在介导对感染的免疫和病原体的清除中的中心作用。
Cell death is a fundamental biological phenomenon that is essential for the survival and development of an organism. Emerging evidence also indicate that cell death contributes to immune defense against infectious diseases. Pyroptosis is a form of inflammatory programed cell death pathway activated by human and mouse caspase-1, human caspase-4 and caspase-5, or mouse caspase-11. These inflammatory caspases are used by the host to control bacterial, viral, fungal or protozoan pathogens. Pyroptosis requires cleavage and activation of the pore-forming effector protein gasdermin D by inflammatory caspases. Physical rupture of the cell causes release of the pro-inflammatory cytokines IL-1β and IL-18, alarmins and endogenous danger-associated molecular patterns, signifying the inflammatory potential of pyroptosis. Here, we describe the central role of inflammatory caspases and pyroptosis in mediating immunity to infection and clearance of pathogens.