期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2015
卷号：112
期号：2
页码：482-487
DOI：10.1073/pnas.1423486112
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：SignificanceA unique population of Foxp3+CD4+ regulatory T (Treg) cells resides in visceral adipose tissue of lean mice. VAT Tregs are important regulators of local and systemic inflammation and metabolism. Here, we show that the VAT Treg signature is imposed early in life, well before the typical age-dependent expansion of the adipose-tissue Treg population. VAT Tregs in obese mice lose the signature typical of lean individuals but gain an additional set of over- and underrepresented transcripts. In striking parallel to a pathway recently elucidated in adipocytes, the obese mouse VAT Treg signature depends on phosphorylation of a specific residue of PPAR{gamma}. These findings are important to consider in designing drugs to target type 2 diabetes and other features of the "metabolic syndrome." A unique population of Foxp3+CD4+ regulatory T (Treg) cells resides in visceral adipose tissue (VAT) of lean mice, especially in the epididymal fat depot. VAT Tregs are unusual in their very high representation within the CD4+ T-cell compartment, their transcriptome, and their repertoire of antigen-specific T-cell receptors. They are important regulators of local and systemic inflammation and metabolism. The overall goal of this study was to learn how the VAT Treg transcriptome adapts to different stimuli; in particular, its response to aging in lean mice, to metabolic perturbations associated with obesity, and to certain signaling events routed through PPAR{gamma
关键词：obesity ; inflammation ; type 2 diabetes ; regulatory T cell ; Foxp3
