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Adipocyte. 2014 Jan 1;3(1):58-62. doi: 10.4161/adip.26220. Epub 2013 Aug 28.

The immune cell transcription factor T-bet: A novel metabolic regulator.

Author information

1
Division of Diabetes and Nutritional Sciences; Department of Experimental Immunobiology; King's College London; London, UK.
2
Department of Experimental Immunobiology; King's College London; London, UK.

Abstract

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-γ-deficient backgrounds indicate the importance of CD4(+) T cells and IFN-γ 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.

KEYWORDS:

IFN-γ; T-bet; Th1; adipose; diabetes; immune; immunometabolism; inflammation; insulin resistance; metabolism; obesity

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