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The effects of cytokines on suppression of lymphocyte proliferation by dexamethasone

Tom J Creed1, Richard W Lee, Paul V Newcomb

  • 1University of Bristol, United Kingdom.

Journal of Immunology (Baltimore, Md. : 1950)
|June 23, 2009
PubMed

Insights

Steroid treatment fails in many inflammatory diseases. This study found Interleukin-2 (IL-2) reduces steroid sensitivity, suggesting IL-2 inhibition could improve treatment outcomes for non-responsive patients.

Area of Science:

  • Immunology
  • Pharmacology

Background:

  • Steroid therapy is crucial for inflammatory diseases but faces treatment failure in up to 30% of patients.
  • Understanding the role of cytokines in steroid resistance is key to improving therapeutic efficacy.

Purpose of the Study:

  • To investigate the involvement of 21 cytokines in steroid-resistant inflammatory conditions.
  • To explore methods for restoring steroid sensitivity via cytokine modulation.

Main Methods:

  • Utilized a dexamethasone inhibition of lymphocyte proliferation assay to assess steroid sensitivity.
  • Correlated peripheral blood mononuclear cell (PBMC) cytokine production with dexamethasone's inhibitory effect (Imax) in healthy volunteers.
  • Investigated exogenous cytokine effects on steroid resistance and cytokine blockade effects on steroid sensitivity in patients with steroid-resistant ulcerative colitis (UC).

Main Results:

  • Production of IL-1α, IL-10, IL-17, IFN-γ, G-CSF, GM-CSF, TNF-α, and IP-10 correlated with in vitro steroid sensitivity.
  • Exogenous IL-2 and TNF-α reduced steroid sensitivity, while IL-10 enhanced it.
  • Blocking IL-2, but not other tested cytokines, improved steroid sensitivity in PBMCs from steroid-resistant UC patients.

Conclusions:

  • IL-2 exhibits a significant antagonistic effect on the antiproliferative action of steroids.
  • Targeting IL-2 may represent a viable strategy to enhance steroid responsiveness in patients with steroid-resistant inflammatory diseases.

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