期刊
CELL METABOLISM
卷 27, 期 3, 页码 588-+出版社
CELL PRESS
DOI: 10.1016/j.cmet.2018.02.007
关键词
-
资金
- British Heart Foundation [FS/13/49/30421, PG/16/79/32419, FS/14/66/31293]
- Marie Curie/Cascade [CF-2013-11-003-longhi]
- Action Against Cancer [PS8508]
- Hilary Craft Foundation [PS8508]
- MRC [MR/L002345/1]
- Medical College of Saint Bartholomew's Hospital Trust
- Bart's and the London School of Medicine
- MRC [MR/R022836/1, MR/L002345/2, MR/L002345/1] Funding Source: UKRI
- Action Medical Research [2272] Funding Source: researchfish
- British Heart Foundation [PG/16/79/32419, FS/13/49/30421] Funding Source: researchfish
- Medical Research Council [MR/L002345/1, MR/R022836/1, MR/L002345/2] Funding Source: researchfish
Visceral adipose tissue (VAT) has multiple roles in orchestrating whole-body energy homeostasis. In addition, VAT is now considered an immune site harboring an array of innate and adaptive immune cells with a direct role in immune surveillance and host defense. We report that conventional dendritic cells (cDCs) in VAT acquire a tolerogenic phenotype through upregulation of pathways involved in adipocyte differentiation. While activation of the Wnt/beta-catenin pathway in cDC1 DCs induces IL-10 production, upregulation of the PPAR gamma pathway in cDC2 DCs directly suppresses their activation. Combined, they promote an anti-inflammatory milieu in vivo delaying the onset of obesity-induced chronic inflammation and insulin resistance. Under long-term over-nutrition, changes in adipocyte biology curtail beta-catenin and PPARg activation, contributing to VAT inflammation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据