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dc.contributor.authorPurton, JF
dc.contributor.authorZhan, YF
dc.contributor.authorLiddicoat, DR
dc.contributor.authorHardy, CL
dc.contributor.authorLew, AM
dc.contributor.authorCole, TJ
dc.contributor.authorGodfrey, DI
dc.date.available2014-05-21T19:30:39Z
dc.date.issued2002-12-01
dc.identifierhttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000179907000023&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=d4d813f4571fa7d6246bdc0dfeca3a1c
dc.identifier.citationPurton, J. F., Zhan, Y. F., Liddicoat, D. R., Hardy, C. L., Lew, A. M., Cole, T. J. & Godfrey, D. I. (2002). Glucocorticoid receptor deficient thymic and peripheral T cells develop normally in adult mice. EUROPEAN JOURNAL OF IMMUNOLOGY, 32 (12), pp.3546-3555. https://doi.org/10.1002/1521-4141(200212)32:12<3546::AID-IMMU3546>3.0.CO;2-S.
dc.identifier.issn0014-2980
dc.identifier.urihttp://hdl.handle.net/11343/26388
dc.descriptionC1 - Journal Articles Refereed
dc.description.abstractThe involvement of glucocorticoid receptor (GR) signaling in T cell development is highly controversial, with several studies for and against. We have previously demonstrated that GR(-/-) mice, which usually die at birth because of impaired lung development, exhibit normal T cell development, at least in embryonic mice and in fetal thymus organ cultures. To directly investigate the role of GR signaling in adult T cell development, we analyzed the few GR(-/-) mice that occasionally survive birth, and irradiated mice reconstituted with GR(-/-) fetal liver precursors. All thymic and peripheral T cells, as well as other leukocyte lineages, developed and were maintained at normal levels. Anti-CD3-induced cell death of thymocytes in vitro, T cell repertoire heterogeneity and T cell proliferation in response to anti-CD3 stimulation were normal in the absence of GR signaling. Finally, we show that metyrapone, an inhibitor of glucocorticoid synthesis (commonly used to demonstrate a role for glucocorticoids in T cell development), impaired thymocyte development regardless of GR genotype indicating that this reagent inhibits thymocyte development in a glucocorticoid-independent fashion. These data demonstrate that GR signaling is not required for either normal T cell development or peripheral maintenance in embryonic or adult mice.
dc.formatapplication/pdf
dc.languageEnglish
dc.publisherWILEY-V C H VERLAG GMBH
dc.subjectCellular Immunology; Biological Sciences
dc.titleGlucocorticoid receptor deficient thymic and peripheral T cells develop normally in adult mice
dc.typeJournal Article
dc.identifier.doi10.1002/1521-4141(200212)32:12<3546::AID-IMMU3546>3.0.CO;2-S
melbourne.peerreviewPeer Reviewed
melbourne.affiliationThe University of Melbourne
melbourne.affiliation.departmentBiochemistry And Molecular Biology
melbourne.source.titleEUROPEAN JOURNAL OF IMMUNOLOGY
melbourne.source.volume32
melbourne.source.issue12
melbourne.source.pages3546-3555
dc.research.coderfcd320202
dc.research.codeseo1998780105
melbourne.publicationid10410
melbourne.elementsid252811
melbourne.contributor.authorLIDDICOAT, DOUGLAS
melbourne.contributor.authorGodfrey, Dale
melbourne.contributor.authorLew, Andrew
melbourne.contributor.authorZhan, Yifan
melbourne.contributor.authorPURTON, JARED
melbourne.contributor.authorCOLE, TIMOTHY
dc.identifier.eissn1521-4141
melbourne.accessrightsThis item is currently not available from this repository


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