Human NLRP3 inflammasome activation is Nox1-4 independent

被引：160

作者：

van Bruggen, Robin ^{[1
,2
]}

Koker, M. Yavuz ^{[3
,4
]}

Jansen, Machiel ^{[2
]}

van Houdt, Michel ^{[2
]}

Roos, Dirk ^{[2
]}

Kuijpers, Taco W. ^{[5
]}

van den Berg, Timo K. ^{[2
]}

机构：

[1] Sanquin Res, Dept Blood Cell Res, NL-1066 CX Amsterdam, Netherlands

[2] Univ Amsterdam, Acad Med Ctr, Landsteiner Lab, NL-1105 AZ Amsterdam, Netherlands

[3] Erciyes Univ, Immunol Lab, Kayseri, Turkey

[4] Erciyes Univ, Cappadocia Transplant Ctr, Kayseri, Turkey

[5] Univ Amsterdam, Acad Med Ctr, Emma Childrens Hosp, NL-1105 AZ Amsterdam, Netherlands

来源：

BLOOD | 2010年 / 115卷 / 26期

关键词：

D O I：

10.1182/blood-2009-10-250803

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The NLRP3 inflammasome can be activated by pathogen-associated molecular patterns or endogenous danger-associated molecular patterns. The activation of the NLRP3 inflammasome results in proteolytic activation and secretion of cytokines of the interleukin-1 (IL-1) family. The precise mode of activation of the NLRP3 inflammasome is still elusive, but has been postulated to be mediated by reactive oxygen species (ROS) generated by an NADPH oxidase. Using primary cells from chronic granulomatous disease (CGD) patients lacking expression of p22(phox), a protein that is required for the function of Nox1-4, we show that cells lacking NADPH oxidase activity are capable of secreting normal amounts of IL-1 beta. Thus, we provide evidence that activation of the NLRP3 inflammasome does not depend on ROS generated from an NADPH oxidase. (Blood. 2010; 115(26):5398-5400)

引用

页码：5398 / 5400

页数：3

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