引发和溶酶体损伤对 NLRP3 激活的关键作用。
Critical functions of priming and lysosomal damage for NLRP3 activation.
机构信息
Institute for Clinical Chemistry and Pharmacology, University Hospital, University of Bonn, Bonn, Germany.
出版信息
Eur J Immunol. 2010 Mar;40(3):620-3. doi: 10.1002/eji.200940185.
Abstract
Inflammasomes are cytosolic multi-protein complexes that form in response to infectious or injurious challenges. Inflammasomes control the activity of caspase-1, which is essential for the maturation and release of IL-1beta family cytokines. The NLRP1, IPAF and AIM2 inflammasomes recognize specific substances, while the NLRP3 inflammasome responds to many structurally and chemically diverse triggers. Here, we discuss the critical roles of priming and lysosomal damage in NLRP3 inflammasome activation.
摘要
炎症小体是细胞浆中的多蛋白复合物，在对感染或损伤的挑战作出反应时形成。炎症小体控制半胱天冬酶-1 的活性，这对半胱天冬酶-1 家族细胞因子的成熟和释放至关重要。NLRP1、IPAF 和 AIM2 炎症小体识别特定物质，而 NLRP3 炎症小体对许多结构和化学上不同的触发物作出反应。在这里，我们讨论了启动和溶酶体损伤在 NLRP3 炎症小体激活中的关键作用。
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本文引用的文献
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