Journal
NATURE MEDICINE
Volume 15, Issue 8, Pages 930-U137Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.2002
Keywords
-
Funding
- Young Chair funds
- US National Institutes of Health [DK51729, DK73547, T32 DK7260]
- Adler Chair funds
- Joslin's National Institutes of Diabetes and Digestive and Kidney Diseases-funded Diabetes and Endocrinology Research Center core facilities
- German Research Foundation [FE 801/1-1]
- Charles A. King Trust Postdoctoral Fellowship
- Ministry of Science of Spain
- European School of Molecular Medicine, respectively
Ask authors/readers for more resources
Obesity is accompanied by chronic, low-grade inflammation of adipose tissue, which promotes insulin resistance and type-2 diabetes. These findings raise the question of how fat inflammation can escape the powerful armamentarium of cells and molecules normally responsible for guarding against a runaway immune response. CD4(+) Foxp3(+) T regulatory (T-reg) cells with a unique phenotype were highly enriched in the abdominal fat of normal mice, but their numbers were strikingly and specifically reduced at this site in insulin-resistant models of obesity. Loss-of-function and gain-of-function experiments revealed that these T-reg cells influenced the inflammatory state of adipose tissue and, thus, insulin resistance. Cytokines differentially synthesized by fat-resident regulatory and conventional T cells directly affected the synthesis of inflammatory mediators and glucose uptake by cultured adipocytes. These observations suggest that harnessing the anti-inflammatory properties of T-reg cells to inhibit elements of the metabolic syndrome may have therapeutic potential. (C) 2009 Nature America, Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available