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Related Experiment Videos

Dexamethasone enhances CTLA-4 expression during T cell activation.

M Xia1, J Gasser, U Feige

  • 1Department of Pharmacology, Amgen Inc., Thousand Oaks, California 91329-1789, USA.

Cellular and Molecular Life Sciences : CMLS
|October 20, 1999
PubMed
Summary

Dexamethasone, an immunosuppressive drug, was found to increase cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) expression during T cell activation. This finding suggests a novel mechanism for how dexamethasone influences immune responses.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Pharmacology

Background:

  • T cell activation relies on costimulatory signals, such as B7-CD28 interaction, promoting proliferation and cytokine production.
  • Cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) is a T cell receptor homologous to CD28, binding B7 ligands with higher affinity and acting as a negative regulator.
  • CTLA-4 expression is transiently observed on activated T cells, playing a role in immune response modulation.

Purpose of the Study:

  • To investigate the kinetics of CTLA-4 expression during T cell activation.
  • To determine the effect of dexamethasone on CTLA-4 expression in activated mouse T cells.
  • To elucidate the mechanism underlying dexamethasone's influence on CTLA-4 expression.

Main Methods:

  • Mouse spleen cells were stimulated using anti-CD3/anti-CD28 monoclonal antibodies or concanavalin A.

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  • CTLA-4 expression levels were monitored over time.
  • Dexamethasone's effects were assessed in a dose-dependent manner, with comparisons to other immunosuppressants like rapamycin and cyclosporin A.
  • Western blot and ribonuclease protection assays were used to quantify CTLA-4 protein and mRNA levels.
  • The role of the glucocorticoid receptor was examined using mifepristone (RU486).

    • Main Results:

    • CTLA-4 expression peaked on day 2 and returned to baseline by day 7.
    • Dexamethasone significantly potentiated CTLA-4 expression in a dose-dependent manner (EC50 ~10(-8) M).
    • Rapamycin had no effect, while cyclosporin A inhibited CTLA-4 expression.
    • Dexamethasone increased both CTLA-4 protein and mRNA levels twofold.
    • The dexamethasone-induced increase in CTLA-4 expression was glucocorticoid-specific and blocked by mifepristone.

    Conclusions:

    • Dexamethasone enhances CTLA-4 expression during T cell activation via the glucocorticoid receptor.
    • This upregulation of CTLA-4 by dexamethasone may contribute to its immunosuppressive effects by downregulating T cell activation.
    • The findings reveal a novel mechanism of action for dexamethasone in immune modulation.