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COPs and POPs patrol inflammasome activation

机译:缔约方会议和持久性有机污染物巡逻炎症小体激活

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摘要

Sensing and responding to pathogens and tissue damage is a core mechanism of innate immune host defense and inflammasomes represent a central cytosolic pattern recognition receptor (PRR) pathway leading to the generation of the pro-inflammatory cytokines IL-1β and IL-18 and pyroptotic cell death that causes the subsequent release of danger signals to propagate and perpetuate inflammatory responses. While inflammasome activation is essential for host defense, deregulated inflammasome responses and excessive release of inflammatory cytokines and danger signals are linked to an increasing spectrum of inflammatory diseases. In this review, we will discuss recent developments in elucidating the role of PYRIN domain-only proteins (POPs) and the related CARD-only proteins (COPs) in regulating inflammasome responses and their impact on inflammatory disease.
机译:对病原体和组织损伤的感知和响应是先天性免疫宿主防御的核心机制,而炎症小体代表了一种中央胞质模式识别受体(PRR)途径,导致促炎性细胞因子IL-1β和IL-18和焦磷酸化细胞的产生死亡,导致随后释放危险信号,从而传播并永久维持炎症反应。尽管炎性体激活对于宿主防御至关重要,但炎性体反应失调以及炎性细胞因子和危险信号的过度释放与越来越多的炎性疾病有关。在这篇综述中,我们将讨论阐明仅PYRIN结构域蛋白(POPs)和相关的仅CARD蛋白(COPs)在调节炎症小体反应及其对炎性疾病影响中的最新进展。

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