Depletion of fat-resident Treg cells prevents age-associated insulin resistance

Sagar P. Bapat, Jae Myoung Suh, Sungsoon Fang, Sihao Liu, Yang Zhang, Albert Cheng, Carmen Zhou, Yuqiong Liang, Mathias LeBlanc, Christopher Liddle, Annette R. Atkins, Ruth T. Yu, Michael Downes, Ronald M. Evans () and Ye Zheng ()
Additional contact information
Sagar P. Bapat: Immunobiology and Microbial Pathogenesis Laboratory, The Salk Institute for Biological Studies
Jae Myoung Suh: Gene Expression Laboratory, The Salk Institute for Biological Studies
Sungsoon Fang: Gene Expression Laboratory, The Salk Institute for Biological Studies
Sihao Liu: Gene Expression Laboratory, The Salk Institute for Biological Studies
Yang Zhang: Immunobiology and Microbial Pathogenesis Laboratory, The Salk Institute for Biological Studies
Albert Cheng: Immunobiology and Microbial Pathogenesis Laboratory, The Salk Institute for Biological Studies
Carmen Zhou: Immunobiology and Microbial Pathogenesis Laboratory, The Salk Institute for Biological Studies
Yuqiong Liang: Immunobiology and Microbial Pathogenesis Laboratory, The Salk Institute for Biological Studies
Mathias LeBlanc: Gene Expression Laboratory, The Salk Institute for Biological Studies
Christopher Liddle: Storr Liver Centre, Westmead Millennium Institute, Sydney Medical School, University of Sydney
Annette R. Atkins: Gene Expression Laboratory, The Salk Institute for Biological Studies
Ruth T. Yu: Gene Expression Laboratory, The Salk Institute for Biological Studies
Michael Downes: Gene Expression Laboratory, The Salk Institute for Biological Studies
Ronald M. Evans: Gene Expression Laboratory, The Salk Institute for Biological Studies
Ye Zheng: Immunobiology and Microbial Pathogenesis Laboratory, The Salk Institute for Biological Studies

Nature, 2015, vol. 528, issue 7580, 137-141

Abstract: Fat-resident regulatory T cells (fTreg cells) accumulate in adipose tissue of mice as a function of age, but not obesity; mice without fTreg cells are protected against age-associated insulin resistance, but remain susceptible to obesity-associated insulin resistance and metabolic disease, indicating different aetiologies of age-associated versus obesity-associated insulin resistance.

Date: 2015
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DOI: 10.1038/nature16151

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