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本文引用的文献

1
Critical functions of priming and lysosomal damage for NLRP3 activation.引发和溶酶体损伤对 NLRP3 激活的关键作用。
Eur J Immunol. 2010 Mar;40(3):620-3. doi: 10.1002/eji.200940185.
2
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.
3
Inflammasomes as microbial sensors.炎症小体作为微生物感应器。
Eur J Immunol. 2010 Mar;40(3):611-5. doi: 10.1002/eji.200940180.
4
Necrotic cells trigger a sterile inflammatory response through the Nlrp3 inflammasome.坏死细胞通过 NLRP3 炎性小体引发无菌性炎症反应。
Proc Natl Acad Sci U S A. 2009 Dec 1;106(48):20388-93. doi: 10.1073/pnas.0908698106. Epub 2009 Nov 16.
5
Activation of the NLRP3 inflammasome in dendritic cells induces IL-1beta-dependent adaptive immunity against tumors.树突状细胞中NLRP3炎性小体的激活诱导针对肿瘤的白细胞介素-1β依赖性适应性免疫。
Nat Med. 2009 Oct;15(10):1170-8. doi: 10.1038/nm.2028. Epub 2009 Sep 20.
6
Rationale for IL-1beta targeted therapy for ischemia-reperfusion induced pulmonary and other complications in sickle cell disease.白细胞介素-1β靶向治疗镰状细胞病缺血再灌注所致肺部及其他并发症的理论依据。
J Pediatr Hematol Oncol. 2009 Aug;31(8):537-8. doi: 10.1097/MPH.0b013e3181acd89d.
7
Biglycan, a danger signal that activates the NLRP3 inflammasome via toll-like and P2X receptors.双糖链蛋白聚糖,一种通过Toll样受体和P2X受体激活NLRP3炎性小体的危险信号。
J Biol Chem. 2009 Sep 4;284(36):24035-48. doi: 10.1074/jbc.M109.014266. Epub 2009 Jul 15.
8
Cutting edge: Necrosis activates the NLRP3 inflammasome.前沿:坏死激活NLRP3炎性小体。
J Immunol. 2009 Aug 1;183(3):1528-32. doi: 10.4049/jimmunol.0901080. Epub 2009 Jul 13.
9
Systematic review and stratified meta-analysis of the efficacy of interleukin-1 receptor antagonist in animal models of stroke.白细胞介素-1受体拮抗剂在中风动物模型中疗效的系统评价和分层荟萃分析
J Stroke Cerebrovasc Dis. 2009 Jul-Aug;18(4):269-76. doi: 10.1016/j.jstrokecerebrovasdis.2008.11.009.
10
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.

NLRP3 炎性小体介导的无菌性炎症反应。

Sterile inflammatory responses mediated by the NLRP3 inflammasome.

机构信息

Division of Allergy and Immunology, Department of Internal Medicine, University of Iowa, Iowa City, IA, USA.

出版信息

Eur J Immunol. 2010 Mar;40(3):607-11. doi: 10.1002/eji.200940207.

DOI:10.1002/eji.200940207
PMID:20201012
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3601805/
Abstract

Through pattern recognition receptors the innate immune system detects disruption of the normal function of the organism and initiates responses directed at correcting these derangements. Cellular damage from microbial or non-microbial insults causes the activation of nucleotide-binding domain leucine-rich repeat containing receptors in multiprotein complexes called inflammasomes. Here we discuss the role of the NLRP3 inflammasome in the recognition of cellular damage and the initiation of sterile inflammatory responses.

摘要

通过模式识别受体,先天免疫系统检测到机体正常功能的破坏,并启动旨在纠正这些异常的反应。微生物或非微生物损伤导致核苷酸结合域富含亮氨酸重复序列受体在多蛋白复合物(称为炎性小体)中的激活。在这里,我们讨论了 NLRP3 炎性小体在识别细胞损伤和启动无菌性炎症反应中的作用。