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

M Feuerer, L Herrero, D Cipolletta, A Naaz, J Wong… - Nature medicine, 2009 - nature.com
M Feuerer, L Herrero, D Cipolletta, A Naaz, J Wong, A Nayer, J Lee, AB Goldfine, C Benoist…
Nature medicine, 2009nature.com
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
(Treg) 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 …
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 (Treg) 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 Treg 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 Treg cells to inhibit elements of the metabolic syndrome may have therapeutic potential.
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