Journal article

Glucocorticoid-mediated repression of T-cell receptor signalling is impaired in glucocorticoid receptor exon 2-disrupted mice

Douglas R Liddicoat, Jared F Purton, Timothy J Cole, Dale I Godfrey



Studies using glucocorticoid receptor exon 2-disrupted knockout (GR2KO) mice provided strong evidence against an obligatory role for glucocorticoid receptor (GR) signalling in T-cell selection. These mice express a truncated form of the GR that is incapable of transmitting a range of glucocorticoid (GC)-induced signals, including GC-induced thymocyte death. However, one study that suggested that truncated GR function is preserved in the context of GR-mediated repression of T-cell activation-induced genes, challenged earlier conclusions derived from the use of these mice. Because GR versus T-cell receptor (TCR) signalling cross-talk is the means by which GCs are hypothesized to have a role in..

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University of Melbourne Researchers


Awarded by National Health and Medical Research Council (NHMRC) of Australia

Awarded by NHMRC Senior Principal Research Fellowship

Funding Acknowledgements

The authors thank Daniel Pellicci and Konstantinos Kyparissoudis for technical help, Max Walker and David Taylor and staff for animal husbandry assistance, and Morag Young for critical comments on the manuscript. We also thank the Picchi Brothers Foundation for generously supporting our flow cytometry facility. This research was supported by a project grant (#350302) from the National Health and Medical Research Council (NHMRC) of Australia. DIG is supported by an NHMRC Senior Principal Research Fellowship (#1020770). This work is dedicated to the memory of Jared F. Purton.