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뇌과학이미징연구단
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Regulation of Chitinase-3-like-1 in T cell elicits Th1 and cytotoxic responses to inhibit lung metastasis

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dc.contributor.authorDo-Hyun Kim-
dc.contributor.authorHong-Jai Park-
dc.contributor.authorSangho Lim-
dc.contributor.authorJa-Hyun Koo-
dc.contributor.authorHong-Gyun Lee-
dc.contributor.authorJin Ouk Choi-
dc.contributor.authorJi Hoon Oh-
dc.contributor.authorSang-Jun Ha-
dc.contributor.authorMin-Jong Kang-
dc.contributor.authorChang-Min Lee-
dc.contributor.authorChun Geun Lee-
dc.contributor.authorJack A. Elias-
dc.contributor.authorJe-Min Choi-
dc.date.available2018-04-27T06:31:19Z-
dc.date.created2018-03-29-
dc.date.issued2018-02-
dc.identifier.issn2041-1723-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/4446-
dc.description.abstractChitinase-3-like-1 (Chi3l1) is known to play a significant role in the pathogenesis of Type 2 inflammation and cancer. However, the function of Chi3l1 in T cell and its clinical implications are largely unknown. Here we show that Chi3l1 expression was increased in activated T cells, especially in Th2 cells. In addition, Chi3l1-deficient T cells are hyper-responsive to TcR stimulation and are prone to differentiating into Th1 cells. Chi3l1-deficient Th1 cells show increased expression of anti-tumor immunity genes and decreased Th1 negative regulators. Deletion of Chi3l1 in T cells in mice show reduced melanoma lung metastasis with increased IFNγ and TNFα-producing T cells in the lung. Furthermore, silencing of Chi3l1 expression in the lung using peptide-siRNA complex (dNP2-siChi3l1) efficiently inhibit lung metastasis with enhanced Th1 and CTL responses. Collectively, this study demonstrates Chi3l1 is a regulator of Th1 and CTL which could be a therapeutic target to enhance anti-tumor immunity.-
dc.description.uri1-
dc.language영어-
dc.publisherNATURE PUBLISHING GROUP-
dc.titleRegulation of Chitinase-3-like-1 in T cell elicits Th1 and cytotoxic responses to inhibit lung metastasis-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000424092000005-
dc.identifier.scopusid2-s2.0-85041668451-
dc.identifier.rimsid63191ko
dc.date.tcdate2018-10-01-
dc.contributor.affiliatedAuthorJe-Min Choi-
dc.identifier.doi10.1038/s41467-017-02731-6-
dc.identifier.bibliographicCitationNATURE COMMUNICATIONS, v.9, no.1, pp.503-
dc.citation.titleNATURE COMMUNICATIONS-
dc.citation.volume9-
dc.citation.number1-
dc.citation.startPage503-
dc.date.scptcdate2018-10-01-
dc.description.wostc1-
dc.description.scptc1-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.subject.keywordPlus3-LIKE 1-
dc.subject.keywordPlusINTERFERON-GAMMA-
dc.subject.keywordPlusNUCLEAR-LOCALIZATION-
dc.subject.keywordPlusTUMOR ANGIOGENESIS-
dc.subject.keywordPlusCOLORECTAL-CANCER-
dc.subject.keywordPlusTISSUE RESPONSES-
dc.subject.keywordPlusBREAST-CANCER-
dc.subject.keywordPlusMYELOID CELLS-
dc.subject.keywordPlusCATHEPSIN-E-
dc.subject.keywordPlusINFLAMMATION-
Appears in Collections:
Center for Neuroscience Imaging Research (뇌과학 이미징 연구단) > 1. Journal Papers (저널논문)
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