Journal
CELL METABOLISM
Volume 26, Issue 3, Pages 475-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2017.08.008
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Funding
- Technische Universitat Munchen - Institute for Advanced Study
- German Excellence Initiative
- European Union [291763]
- Research Group at Helmholtz Zentrum Munchen
- German Center for Diabetes Research (DZD)
- Deutsche Forschungsgemeinschaft [CRC1054]
- Public Health Services award [AI095282]
- Alexander von Humboldt Foundation
- DZD
- Helmholtz Alliance ICEMED
- Helmholtz Initiative on Personalized Medicine iMed by Helmholtz Association
- Helmholtz cross-program topic Metabolic Dysfunction
- [WE 4656/2]
- [DFG-CRC1181]
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Obesity and type 2 diabetes are associated with metabolic defects and adipose tissue inflammation. Foxp3(+) regulatory T cells (Tregs) control tissue homeostasis by counteracting local inflammation. However, if and how T cells interlink environmental influences with adipocyte function remains unknown. Here, we report that enhancing sympathetic tone by cold exposure, beta3-adrenergic receptor (ADRB3) stimulation or a short-term high-calorie diet enhances Treg induction in vitro and in vivo. CD4(+) T cell proteomes revealed higher expression of Foxp3 regulatory networks in response to cold or ADRB3 stimulation in vivo reflecting Treg induction. Specifically, Ragulator-interacting protein C17orf59, which limits mTORC1 activity, was upregulated in CD4(+) T cells by either ADRB3 stimulation or cold exposure, suggesting contribution to Treg induction. By loss-and gain-of-function studies, including Treg depletion and transfers in vivo, we demonstrated that a T cell-specific Stat6/Pten axis links cold exposure or ADRB3 stimulation with Foxp3(+) Treg induction and adipose tissue function. Our findings offer a new mechanistic model in which tissue-specific Tregs maintain adipose tissue function.
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