CXCR3 Controls T-Cell Accumulation in Fat Inflammation
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Rocha, V. Z.
Tang, E. H. C.
Bittencourt, M. S.
Santos, R. D.
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CitationRocha, V. Z., E. J. Folco, C. Ozdemir, Y. Sheikine, T. Christen, G. K. Sukhova, E. H. C. Tang, et al. 2014. “CXCR3 Controls T-Cell Accumulation in Fat Inflammation.” Arteriosclerosis, Thrombosis, and Vascular Biology 34 (7) (May 8): 1374–1381. doi:10.1161/atvbaha.113.303133.
AbstractObjective—Obesity associates with increased numbers of inflammatory cells in adipose tissue (AT), including T cells, but the mechanism of T-cell recruitment remains unknown. This study tested the hypothesis that the chemokine receptor CXCR3 participates in T-cell accumulation in AT of obese mice and thus in the regulation of local inflammation and systemic metabolism.
Approach and Results—Obese wild-type mice exhibited higher mRNA expression of CXCR3 in periepididymal AT-derived stromal vascular cells compared with lean mice. We evaluated the function of CXCR3 in AT inflammation in vivo using CXCR3-deficient and wild-type control mice that consumed a high-fat diet. Periepididymal AT from obese CXCR3-deficient mice contained fewer T cells than obese controls after 8 and 16 weeks on high-fat diet, as assessed by flow cytometry. Obese CXCR3-deficient mice had greater glucose tolerance than obese controls after 8 weeks, but not after 16 weeks. CXCR3-deficient mice fed high-fat diet had reduced mRNA expression of proinflammatory mediators, such as monocyte chemoattractant protein-1 and regulated on activation, normal T cell expressed and secreted, and anti-inflammatory genes, such as Foxp3, IL-10, and arginase-1 in periepididymal AT, compared with obese controls.
Conclusions—These results demonstrate that CXCR3 contributes to T-cell accumulation in periepididymal AT of obese mice. Our results also suggest that CXCR3 regulates the accumulation of distinct subsets of T cells and that the ratio between these functional subsets across time likely modulates local inflammation and systemic metabolism.
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