The modern interleukin-1 superfamily: Divergent roles in obesity

被引：29
作者：
Lee, Man K. S. [1 ,2 ]
Yvan-Charvet, Laurent [3 ]
Masters, Seth L. [4 ]
Murphy, Andrew J. [1 ,2 ]
机构：
[1] Baker IDI Heart & Diabet Inst, Haematopoiesis & Leukocyte Biol, Melbourne, Vic 3004, Australia
[2] Monash Univ, Dept Immunol, Melbourne, Vic 3004, Australia
[3] Inst Natl Sante & Rech Med INSERM U01065, C3M, Nice, France
[4] Walter & Eliza Hall Inst Med Res, Inflammat Div, Parkville, Vic 3052, Australia
来源：
SEMINARS IN IMMUNOLOGY | 2016年 / 28卷 / 05期
基金：
澳大利亚国家健康与医学研究理事会;
关键词：
IL-1; beta; IL-18; IL-33; Obesity; Cytokines; Fatty acid oxidation; RECEPTOR ACCESSORY PROTEIN; NF-KAPPA-B; ADIPOSE-TISSUE; NLRP3; INFLAMMASOME; GAMMA-INTERFERON; MACROPHAGE ACCUMULATION; ORCHESTRATE DEVELOPMENT; ENERGY-EXPENDITURE; GENE POLYMORPHISM; STRUCTURAL BASIS;
D O I：
10.1016/j.smim.2016.10.001
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Obesity is now recognised as a chronic, low-grade inflammatory disease contributing to insulin resistance, type 2 diabetes (T2D) and cardiovascular disease (CVD). Multiple mechanisms leading to the low grade inflammation in this setting have been suggested. Due to the complexity and interconnection of inflammatory and metabolic responses, there also remains a need to fully elucidate the inflammatory mechanisms that control obesity and associated metabolic disorders. One important avenue in the field that has gained great attention is the interleukin (IL)-1 superfamily of cytokines that consist of IL-beta, IL-18 and IL-33. IL-1 beta is well known for its contribution as an inflammatory mediator in obesity contributing to insulin resistance and T2D, whereas the IL-18 and IL-33 cytokines have been shown to oppose metabolic dysregulation. This review will focus on the current understanding of the IL-1 superfamily of cytokines in the setting of obesity and discuss how endogenous feedback loops can be exploited for therapeutic approaches to fight obesity and subsequent cardiometabolic disorders. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码：441 / 449
页数：9
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