Glucocorticoid receptor deficient thymic and peripheral T cells develop normally in adult mice
AuthorPurton, JF; Zhan, YF; Liddicoat, DR; Hardy, CL; Lew, AM; Cole, TJ; Godfrey, DI
Source TitleEUROPEAN JOURNAL OF IMMUNOLOGY
PublisherWILEY-V C H VERLAG GMBH
University of Melbourne Author/sLIDDICOAT, DOUGLAS; Godfrey, Dale; Lew, Andrew; Zhan, Yifan; PURTON, JARED; COLE, TIMOTHY
AffiliationBiochemistry And Molecular Biology
Document TypeJournal Article
CitationsPurton, 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.
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C1 - Journal Articles Refereed
The 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.
KeywordsCellular Immunology; Biological Sciences
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