期刊
ADIPOCYTE
卷 3, 期 1, 页码 58-62出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/adip.26220
关键词
T-bet; adipose; obesity; immune; Th1; insulin resistance; inflammation; metabolism; immunometabolism; IFN-gamma; diabetes
资金
- Medical Research Council [MR/K002996/1, G0802068]
- Wellcome Trust [WT091009]
- National Institute for Health Research (NIHR) Biomedical Research Centre based at Guy's and St Thomas' NHS Foundation Trust and King's College London
- MRC [MR/K002996/1, G0802068] Funding Source: UKRI
Obesity-associated insulin resistance is accompanied by an alteration in the Th1/Th2 balance in adipose tissue. T-bet (Tbx21) is an immune cell transcription factor originally described as the master regulator of Th1 cell development, although is now recognized to have a role in both the adaptive and innate immune systems. T-bet also directs T-cell homing to pro-inflammatory sites by the regulation of CXCR3 expression. T-bet(-/-) mice have increased visceral adiposity but are more insulin-sensitive, exhibiting reduced immune cell content and cytokine secretion specifically in the visceral fat depot, perhaps due to altered T-cell trafficking. Studies of T-bet deficiency on Rag2-and IFN-gamma-deficient backgrounds indicate the importance of CD4(+) T cells and IFN-gamma in this model. This favorable metabolic phenotype, uncoupling adiposity from insulin resistance, is present in young lean mice yet persists with age and increasing obesity. We suggest a novel role for T-bet in metabolic regulation.
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