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  -