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Effects of IL-7 and dexamethasone: Induction of CD25, the high affinity IL-2 receptor, on human CD4(+) cells

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dc.contributor.authorChung, Il Yup-
dc.contributor.authorDong, Hui Fang-
dc.contributor.authorZhang, Xia-
dc.contributor.authorHassanein, Nahed M.A.-
dc.contributor.authorHoward, O.M. Zack-
dc.contributor.authorOppenheim, Joost J.-
dc.contributor.authorChen, Xin-
dc.date.accessioned2021-06-24T00:38:57Z-
dc.date.available2021-06-24T00:38:57Z-
dc.date.issued2004-11-
dc.identifier.issn0008-8749-
dc.identifier.issn1090-2163-
dc.identifier.urihttps://scholarworks.bwise.kr/erica/handle/2021.sw.erica/46548-
dc.description.abstractSince we have previously shown that dexamethasone (Dex) enhances the proportion of murine Treg cells, we tested the effect of IL-7, a promoter of T cell survival, together with Dex oil human CD4(+)CD25(+) Treg cells in an in vitro setting. The results showed that IL-7 in concert with Dex markedly augmented the generation of CD4(+)CD25(+) T cells. To discern the origin of the induced CD4(+)CD25(+) T cells, MACS-purified CD4(+)CD25(-), and CD4(+)CD25(+) cells were cultured in the presence of Dex and/or IL-7 for 4 days. Although two thirds of CD4(+)CD25(-) T cells became CD4(+)CD25(+) T cells, they had no Suppressive activity. In contrast, the original CD4(+)CD25(+) T cells maintained Suppressive activity after Dex/IL-7 treatment, however, there was not a significant expansion ill their cell number. Dex and IL-7 did not induce additional Treg cells, but additively induced the expression of the activation marker CD25 by CD4(+)CD25(-) T cells. This combination may provide a novel means of priming CD4 T cells to respond to IL-2 and may prove useful in up-regulation of normal immune responses in immune deficient diseases. (c) 2005 Elsevier Inc. All rights reserved.-
dc.format.extent7-
dc.language영어-
dc.language.isoENG-
dc.publisherAcademic Press-
dc.titleEffects of IL-7 and dexamethasone: Induction of CD25, the high affinity IL-2 receptor, on human CD4(+) cells-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.1016/j.cellimm.2005.01.011-
dc.identifier.scopusid2-s2.0-19544390873-
dc.identifier.wosid000229764300007-
dc.identifier.bibliographicCitationCellular Immunology, v.232, no.1-2, pp 57 - 63-
dc.citation.titleCellular Immunology-
dc.citation.volume232-
dc.citation.number1-2-
dc.citation.startPage57-
dc.citation.endPage63-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaCell Biology-
dc.relation.journalResearchAreaImmunology-
dc.relation.journalWebOfScienceCategoryCell Biology-
dc.relation.journalWebOfScienceCategoryImmunology-
dc.subject.keywordPlusT-CELLS-
dc.subject.keywordPlusAUTOIMMUNE-DISEASES-
dc.subject.keywordPlusREGULATORY CELLS-
dc.subject.keywordPlusSELF-TOLERANCE-
dc.subject.keywordPlusALPHA GENE-
dc.subject.keywordPlusIN-VITRO-
dc.subject.keywordPlusGLUCOCORTICOIDS-
dc.subject.keywordPlusCD4(+)CD25(+)-
dc.subject.keywordPlusPROLIFERATION-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordAuthorCD4(+) CD25(+) regulatory T lymphocytes-
dc.subject.keywordAuthordexamethasone-
dc.subject.keywordAuthorinterleukin-7-
dc.subject.keywordAuthorsuppression/anergy-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0008874905000225?via%3Dihub-
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