TY - JOUR AU - Purton, JF AU - Zhan, YF AU - Liddicoat, DR AU - Hardy, CL AU - Lew, AM AU - Cole, TJ AU - Godfrey, DI Y2 - 2014/05/21 Y1 - 2002/12/01 SN - 0014-2980 UR - http://hdl.handle.net/11343/26388 AB - 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. N1 - application/pdf LA - English PB - WILEY-V C H VERLAG GMBH KW - Cellular Immunology; Biological Sciences T1 - Glucocorticoid receptor deficient thymic and peripheral T cells develop normally in adult mice DO - 10.1002/1521-4141(200212)32:12<3546::AID-IMMU3546>3.0.CO;2-S IS - EUROPEAN JOURNAL OF IMMUNOLOGY VL - 32 IS - 12 SP - 3546-3555 L1 - /bitstream/handle/11343/26388/116178_5228.pdf?sequence=1&isAllowed=n ER -