期刊
CELL
卷 178, 期 3, 页码 686-+出版社
CELL PRESS
DOI: 10.1016/j.cell.2019.05.054
关键词
-
资金
- Chan Zuckerberg Initiative
- HHMI international scholar award
- European Research Council consolidator grant (ERC-COG) [724471-Hem-Tree2.0]
- Thompson Family Foundation
- MRA established investigator award [509044]
- Israel Science Foundation [703/15]
- Ernest and Bonnie Beutler Research Program for Excellence in Genomic Medicine
- Helen and Martin Kimmel award for innovative investigation
- NeuroMac DFG/Transregional Collaborative Research Center grant
- Adelis Foundation
- SCA award of the Wolfson Foundation
- NIH [DK49780]
- CHOP junior faculty grant
- Center for Applied Genomics at the Children's Hospital of Philadelphia [P30 NIH DK19525]
- Agilent early career professor award
- Global Probiotics Council
- PennCHOP Microbiome Program
- Penn Institute for Immunology
- Penn Center for Molecular Studies in Digestive and Liver Diseases [P30-DK-050306, P30-AR-069589]
- Penn Diabetes Research Center [P30-DK-019525]
- Gilead Sciences International Research Scholars Program in Liver Disease
- Leona M. and Harry B. Helmsley Charitable Trust
- Adelis Foundation - European Research Council
- Helmholtz Foundation
- Bill and Melinda Gates Foundation
- Howard Hughes Medical Institute (HHMI)
- International Progressive MS Alliance/NMSS [PA-1604-08459]
Immune cells residing in white adipose tissue have been highlighted as important factors contributing to the pathogenesis of metabolic diseases, but the molecular regulators that drive adipose tissue immune cell remodeling during obesity remain largely unknown. Using index and transcriptional single-cell sorting, we comprehensively map all adipose tissue immune populations in both mice and humans during obesity. We describe a novel and conserved Trem2(+) lipid-associated macrophage (LAM) subset and identify markers, spatial localization, origin, and functional pathways associated with these cells. Genetic ablation of Trem2 in mice globally inhibits the downstream molecular LAM program, leading to adipocyte hypertrophy as well as systemic hyper-cholesterolemia, body fat accumulation, and glucose intolerance. These findings identify Trem2 signaling as a major pathway by which macrophages respond to loss of tissue-level lipid homeostasis, highlighting Trem2 as a key sensor of metabolic pathologies across multiple tissues and a potential therapeutic target in metabolic diseases.
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