Article abstract


Nature Medicine 15, 930 - 939 (2009)
Published online: 26 July 2009 | doi:10.1038/nm.2002

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

Markus Feuerer1,5, Laura Herrero2,5, Daniela Cipolletta1,4,5, Afia Naaz2, Jamie Wong1,5, Ali Nayer2, Jongsoon Lee2, Allison B Goldfine3, Christophe Benoist1,5, Steven Shoelson2 & Diane Mathis1,5


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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  1. Immunology and Immunogenetics, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
  2. Cellular and Molecular Physiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
  3. Clinical Research, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
  4. European School of Molecular Medicine, Naples, Italy.
  5. Present addresses: Department of Pathology, Harvard Medical School, Boston, Massachusetts, USA (M.F., D.C., C.B. and D.M.); Department of Biochemistry and Molecular Biology, School of Pharmacy, University of Barcelona, Barcelona, Spain (L.H.); Alnylam Pharmaceuticals, Cambridge, Massachusetts, USA (J.W.).

Correspondence to: Diane Mathis1,5 e-mail: dm@hms.harvard.edu



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