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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.

DOI:10.1002/eji.200940185
PMID:20201015
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3893565/
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

1
Signaling by ROS drives inflammasome activation.ROS 通过信号转导驱动炎症小体激活。
Eur J Immunol. 2010 Mar;40(3):616-9. doi: 10.1002/eji.200940168.
2
Malarial hemozoin is a Nalp3 inflammasome activating danger signal.疟原虫血红素是 Nalp3 炎性体激活的危险信号。
PLoS One. 2009 Aug 4;4(8):e6510. doi: 10.1371/journal.pone.0006510.
3
Cutting edge: NF-kappaB activating pattern recognition and cytokine receptors license NLRP3 inflammasome activation by regulating NLRP3 expression.前沿:NF-κB激活模式识别和细胞因子受体通过调节NLRP3表达许可NLRP3炎性小体激活。
J Immunol. 2009 Jul 15;183(2):787-91. doi: 10.4049/jimmunol.0901363. Epub 2009 Jul 1.
4
AIMing 2 detect foreign DNA.旨在检测外源DNA。
Sci Signal. 2009 Jun 30;2(77):pe39. doi: 10.1126/scisignal.277pe39.
5
Cutting edge: TNF-alpha mediates sensitization to ATP and silica via the NLRP3 inflammasome in the absence of microbial stimulation.前沿:在无微生物刺激的情况下,肿瘤坏死因子-α通过NLRP3炎性小体介导对ATP和二氧化硅的致敏作用。
J Immunol. 2009 Jul 15;183(2):792-6. doi: 10.4049/jimmunol.0900173. Epub 2009 Jun 19.
6
Horror autoinflammaticus: the molecular pathophysiology of autoinflammatory disease (*).自身炎症恐怖症:自身炎症性疾病的分子病理生理学(*)
Annu Rev Immunol. 2009;27:621-68. doi: 10.1146/annurev.immunol.25.022106.141627.
7
Immunological and inflammatory functions of the interleukin-1 family.白细胞介素-1家族的免疫和炎症功能。
Annu Rev Immunol. 2009;27:519-50. doi: 10.1146/annurev.immunol.021908.132612.
8
The inflammasomes: guardians of the body.炎性小体:身体的守护者。
Annu Rev Immunol. 2009;27:229-65. doi: 10.1146/annurev.immunol.021908.132715.
9
Uptake of particulate vaccine adjuvants by dendritic cells activates the NALP3 inflammasome.树突状细胞摄取颗粒性疫苗佐剂会激活NALP3炎性小体。
Proc Natl Acad Sci U S A. 2009 Jan 20;106(3):870-5. doi: 10.1073/pnas.0804897106. Epub 2009 Jan 12.
10
Initial description of the human NLRP3 promoter.人类NLRP3启动子的初步描述。
Genes Immun. 2008 Dec;9(8):721-6. doi: 10.1038/gene.2008.66. Epub 2008 Aug 21.