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Differential response of murine CD4(+)CD25(+) and CD4(+)CD25(-) T cells to dexamethasone-induced cell death

  1. Author:
    Chen, X.
    Murakami, T.
    Oppenheim, J. J.
    Howard, D. M. Z.

  2. Author Address

    Howard, DMZ, NCI, Mol Immunoregulat Lab, Ctr Canc Res, POB B,Bldg 560,Room 31-19, Ft Detrick, MD 21702 USA NCI, Mol Immunoregulat Lab, Ctr Canc Res, Ft Detrick, MD 21702 USA. SAIC Frederick Inc, Basic Res Program, Frederick, MD USA.
    1. Year: 2004
  2. Journal: European Journal of Immunology
    1. 34
    2. 3
    3. Pages: 859-869
  4. Type of Article: Article
  1. Abstract:

    To evaluate the in vivo effect of immunosuppressive glucocorticoids on CD4(+)CD25(+) T regulatory cells, we injected dexamethasone (Dex) into BALB/c mice. Administration of 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 the thymus. 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 did not 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

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