Details

Autor(en) / Beteiligte

• Mathis, Diane
• Benoist, Christophe
• Nayer, Ali
• Lee, Jongsoon
• Naaz, Afia
• Shoelson, Steven
• Feuerer, Markus
• Wong, Jamie
• Cipolletta, Daniela
• Herrero, Laura
• Goldfine, Allison B

Titel

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

Ist Teil von

• Nature medicine, 2009-08, Vol.15 (8), p.930-939

Ort / Verlag

New York: Nature Publishing Group US

Erscheinungsjahr

2009

Quelle

MEDLINE

Beschreibungen/Notizen

• In these new reports, three different research groups independently find that various T cell populations are crucial mediators of obesity-induced metabolic dysfunction. They also show that pharmacological approaches that target these T cells are beneficial, thus opening the door to possible new therapeutic approaches to treating obesity-related diseases such as diabetes ( pages 846–847 , 914–920 and 921–929 ). 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.