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Activation of caspase-1 by the NLRP3 inflammasome regulates the NADPH oxidase NOX2 to control phagosome function

机译:NLRP3炎性体激活caspase-1可调节NADPH氧化酶NOX2以控制吞噬功能

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摘要

Phagocytosis is a fundamental cellular process that is pivotal for immunity as it coordinates microbial killing, innate immune activation and antigen presentation. An essential step in this process is phagosome acidification, which regulates many functions of these organelles that allow phagosomes to participate in processes that are essential to both innate and adaptive immunity. Here we report that acidification of phagosomes containing Gram-positive bacteria is regulated by the NLRP3 inflammasome and caspase-1. Active caspase-1 accumulates on phagosomes and acts locally to control the pH by modulating buffering by the NADPH oxidase NOX2. These data provide insight into a mechanism by which innate immune signals can modify cellular defenses and establish a new function for the NLRP3 inflammasome and caspase-1 in host defense.
机译:吞噬作用是基本的细胞过程,对免疫至关重要,因为它可以协调微生物的杀灭,先天免疫激活和抗原呈递。吞噬体酸化是这一过程的重要步骤,它调节了这些细胞器的许多功能,使吞噬体参与了固有免疫和适应性免疫所必需的过程。在这里我们报告说,含有革兰氏阳性细菌的吞噬体的酸化受到NLRP3炎性体和caspase-1的调节。活性caspase-1积聚在吞噬体上,并通过调节NADPH氧化酶NOX2的缓冲作用来局部控制pH。这些数据提供了对先天免疫信号可以修饰细胞防御并在宿主防御中为NLRP3炎性小体和caspase-1建立新功能的机制的深入了解。

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