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Article: CXCR3 controls T cell accumulation in fat accumulation

TitleCXCR3 controls T cell accumulation in fat accumulation
Authors
Keywordsadipose tissue
CXCR3 receptors
inflammation
lymphocytes
macrophages
obesity
Issue Date2014
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.lww.com/product/?1079-5642
Citation
Arteriosclerosis, Thrombosis, and Vascular Biology, 2014, v. 34 n. 7, p. 1374-1381 How to Cite?
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 (C-X-C motif) receptor 3 (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. © 2014 American Heart Association, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/200780
ISSN
2023 Impact Factor: 7.4
2023 SCImago Journal Rankings: 2.582
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRocha, VZ-
dc.contributor.authorSheikine, Y-
dc.contributor.authorChristen, T-
dc.contributor.authorFolco, EJ-
dc.contributor.authorSukhova, G-
dc.contributor.authorTang, EHC-
dc.contributor.authorLuster, A-
dc.contributor.authorLibby, P-
dc.date.accessioned2014-08-21T07:01:04Z-
dc.date.available2014-08-21T07:01:04Z-
dc.date.issued2014-
dc.identifier.citationArteriosclerosis, Thrombosis, and Vascular Biology, 2014, v. 34 n. 7, p. 1374-1381-
dc.identifier.issn1079-5642-
dc.identifier.urihttp://hdl.handle.net/10722/200780-
dc.description.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 (C-X-C motif) receptor 3 (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. © 2014 American Heart Association, Inc.-
dc.languageeng-
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.lww.com/product/?1079-5642-
dc.relation.ispartofArteriosclerosis, Thrombosis, and Vascular Biology-
dc.rightsThis is a non-final version of an article published in final form in (provide complete journal citation)-
dc.subjectadipose tissue-
dc.subjectCXCR3 receptors-
dc.subjectinflammation-
dc.subjectlymphocytes-
dc.subjectmacrophages-
dc.subjectobesity-
dc.titleCXCR3 controls T cell accumulation in fat accumulation-
dc.typeArticle-
dc.identifier.emailTang, EHC: evatang1@hku.hk-
dc.identifier.authorityTang, EHC=rp01382-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1161/ATVBAHA.113.303133-
dc.identifier.pmid24812325-
dc.identifier.pmcidPMC4102314-
dc.identifier.scopuseid_2-s2.0-84903157585-
dc.identifier.hkuros233018-
dc.identifier.volume34-
dc.identifier.issue7-
dc.identifier.spage1374-
dc.identifier.epage1381-
dc.identifier.isiWOS:000337732900012-
dc.publisher.placeUnited States-
dc.identifier.issnl1079-5642-

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