Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect metabolic parameters.
Nat Med, 2009/8;15(8):930-9.
Feuerer M[1], Herrero L, Cipolletta D, Naaz A, Wong J, Nayer A, Lee J, Goldfine AB, Benoist C, Shoelson S, Mathis D
Affiliations
PMID: 19633656DOI: 10.1038/nm.2002
Impact factor: 87.241
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.
MeSH terms
Adipose Tissue; Animals; Cell Proliferation; Cell Separation; Gene Expression Profiling; Lymphocyte Count; Male; Metabolic Networks and Pathways; Mice; Mice, Inbred C57BL; Mice, Obese; Obesity; T-Lymphocytes, Regulatory; Thinness; Up-Regulation
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