Modulatory mechanisms controlling the NLRP3 inflammasome in inflammation: recent developments

被引：242

作者：

Haneklaus, Moritz ^{[1
]}

O'Neill, Luke A. J. ^{[1
]}

Coll, Rebecca C. ^{[1
]}

机构：

[1] Trinity Coll Dublin, Trinity Biomed Sci Inst, Sch Biochem & Immunol, Dublin 2, Ireland

来源：

CURRENT OPINION IN IMMUNOLOGY | 2013年 / 25卷 / 01期

基金：

欧洲研究理事会; 爱尔兰科学基金会;

关键词：

NF-KAPPA-B; NALP3; INFLAMMASOME; ACTIVATION; IL-1-BETA; SECRETION; CRYSTALS; SILICA; CA2+;

D O I：

10.1016/j.coi.2012.12.004

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

The protein NLRP3 has emerged as a central regulator in the inflammatory process, being implicated directly in hereditary cryopyrinopathies, and indirectly in diseases such as gout, Type 2 diabetes and atherosclerosis. NLRP3 is an important regulator of caspase-1, the enzyme that processes the immature form of IL-1 beta into the active protein. The control of NLRP3 has therefore become a focus of research with evidence for redox regulation, ubiquitination and regulation by miRNA-223, kinases and calcium all emerging as controllers of NLRP3. As our knowledge expands the prospect for precise pharmacological targeting of NLRP3 will improve and could lead to substantial clinical utility.

引用

页码：40 / 45

页数：6

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