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T-cell senescence contributes to abnormal glucose homeostasis in humans and mice

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dc.contributor.authorYi, Hyon-Seung-
dc.contributor.authorKim, So Yeon-
dc.contributor.authorKim, Jung Tae-
dc.contributor.authorLee, Young-Sun-
dc.contributor.authorMoon, Ji Sun-
dc.contributor.authorKim, Mingyo-
dc.contributor.authorKang, Yea Eun-
dc.contributor.authorJoung, Kyong Hye-
dc.contributor.authorLee, Ju Hee-
dc.contributor.authorKim, Hyun Jin-
dc.contributor.authorChun, Kwangsik-
dc.contributor.authorShong, Minho-
dc.contributor.authorKu, Bon Jeong-
dc.date.available2020-11-02T06:41:11Z-
dc.date.issued2019-03-
dc.identifier.issn2041-4889-
dc.identifier.urihttps://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/2283-
dc.description.abstractChronic inflammation is a driving force for the development of metabolic disease including diabetes and obesity. However, the functional characteristics of T-cell senescence in the abnormal glucose homeostasis are not fully understood. We studied the patients visiting a hospital for routine health check-ups, who were divided into two groups: normal controls and people with prediabetes. Gene expression profiling of peripheral blood mononuclear cells from normal controls and patients with type 2 diabetes was undertaken using microarray analysis. We also investigated the immunometabolic characteristics of peripheral and hepatic senescent T cells in the normal subjects and patients with prediabetes. Moreover, murine senescent T cells were tested functionally in the liver of normal or mice with metabolic deterioration caused by diet-induced obesity. Human senescent (CD28(-)CD57(+)) CD8(+) T cells are increased in the development of diabetes and proinflammatory cytokines and cytotoxic molecules are highly expressed in senescent T cells from patients with prediabetes. Moreover, we demonstrate that patients with prediabetes have higher concentrations of reactive oxygen species (ROS) in their senescent CD8(+) T cells via enhancing capacity to use glycolysis. These functional properties of senescent CD8(+) T cells contribute to the impairment of hepatic insulin sensitivity in humans. Furthermore, we found an increase of hepatic senescent T cells in mouse models of aging and diet-induced obesity. Adoptive transfer of senescent CD8(+) T cells also led to a significant deterioration in systemic abnormal glucose homeostasis, which is improved by ROS scavengers in mice. This study defines a new clinically relevant concept of T-cell senescence-mediated inflammatory responses in the pathophysiology of abnormal glucose homeostasis. We also found that T-cell senescence is associated with systemic inflammation and alters hepatic glucose homeostasis. The rational modulation of T-cell senescence would be a promising avenue for the treatment or prevention of diabetes.-
dc.language영어-
dc.language.isoENG-
dc.publisherNature Publishing Group-
dc.titleT-cell senescence contributes to abnormal glucose homeostasis in humans and mice-
dc.typeArticle-
dc.publisher.location영국-
dc.identifier.doi10.1038/s41419-019-1494-4-
dc.identifier.scopusid2-s2.0-85062869330-
dc.identifier.wosid000462414000002-
dc.identifier.bibliographicCitationCell Death and Disease, v.10-
dc.citation.titleCell Death and Disease-
dc.citation.volume10-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaCell Biology-
dc.relation.journalWebOfScienceCategoryCell Biology-
dc.subject.keywordPlusINSULIN-RESISTANCE-
dc.subject.keywordPlusADIPOSE-TISSUE-
dc.subject.keywordPlusTRANSCRIPTION FACTOR-
dc.subject.keywordPlusINFLAMMATION-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusCYTOKINES-
dc.subject.keywordPlusRISK-
dc.subject.keywordPlusASSOCIATION-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusRECEPTOR-
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