Abstract
To evaluate the in vivo effect of immunosuppressive glucocorticoids on CD4^+^CD25^+^ T regulatory cells, we injected dexamethasone (Dex) into BALB/c mice. Administrationof Dex enhanced the proportion of CD4^+^CD25^+^ cells and the ratio of CD4^+^CD25^+^ cells to CD4^+^CD25^–^ cells in the lymphoid organs, especially in thethymus. This correlates with our in vitro observation that CD4^+^CD25^+^ T cells express higher levels of glucocorticoid receptor and Bcl‐2, and are therefore more resistant to Dex‐mediated cell death than CD4^+^CD25^–^ T cells. Furthermore, IL‐2 selectively protected CD4^+^CD25^+^ T cells from Dex‐induced cell death, while IL‐7 and IL‐15 didnot exert preferential protective effects. Dex‐treated CD4^+^CD25^+^ T cells expressed higher levels of intracellular CTLA‐4 and surface glucocorticoid‐induced TNF receptor than fresh CD4^+^CD25^+^ T cells, but still failed to respond to TCR stimulation and inhibited proliferation of CD4^+^CD25^–^ T cells. These results suggest that, in addition to suppressing cytokine transcription, Dex treatment is permissive for the survival of functional CD4^+^CD25^+^ T regulatory cells, and this property may contribute to the anti‐inflammatory and immunosuppressive efficacy of glucocorticoids. Our data also suggest that selective protection of CD4^+^CD25^+^ T cell from apoptosis may constitute a role in immune tolerance for IL‐2.