Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect metabolic parameters

Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect... 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Medicine Springer Journals

Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect metabolic parameters

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Publisher
Springer Journals
Copyright
Copyright © 2009 Nature Publishing Group
ISSN
1078-8956
eISSN
1546-170X
DOI
10.1038/nm.2002
pmid
19633656
Publisher site
See Article on Publisher Site

Abstract

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.

Journal

Nature MedicineSpringer Journals

Published: Jul 26, 2009

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