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

Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Joslin Diabetes Center, Boston, Massachusetts, USA.
Nature medicine (Impact Factor: 28.05). 09/2009; 15(8):930-9. DOI: 10.1038/nm.2002
Source: PubMed

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.

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