感知 NLRP3 炎性体的损伤。
Sensing damage by the NLRP3 inflammasome.
机构信息
Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
出版信息
Immunol Rev. 2011 Sep;243(1):152-62. doi: 10.1111/j.1600-065X.2011.01043.x.
Abstract
The NLRP3 inflammasome is activated in response to a variety of signals that are indicative of damage to the host including tissue damage, metabolic stress, and infection. Upon activation, the NLRP3 inflammasome serves as a platform for activation of the cysteine protease caspase-1, which leads to the processing and secretion of the proinflammatory cytokines interleukin-1β (IL-1β) and IL-18. Dysregulated NLRP3 inflammasome activation is associated with both heritable and acquired inflammatory diseases. Here, we review new insights into the mechanism of NLRP3 inflammasome activation and its role in disease pathogenesis.
摘要
NLRP3 炎性小体被激活以响应多种信号，这些信号表明宿主受到损伤，包括组织损伤、代谢应激和感染。激活后，NLRP3 炎性小体充当半胱氨酸蛋白酶 caspase-1 的激活平台，导致促炎细胞因子白细胞介素-1β（IL-1β）和 IL-18 的加工和分泌。NLRP3 炎性小体激活失调与遗传性和获得性炎症性疾病有关。在这里，我们回顾了 NLRP3 炎性小体激活机制及其在疾病发病机制中的作用的新见解。
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