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c-Rel is a target of pentoxifylline-mediated inhibition of T lymphocyte activation

W Wang1, W F Tam, C C Hughes

  • 1Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02254, USA.

Immunity
|February 1, 1997
PubMed

Insights

Pentoxifylline (PF) selectively blocks c-Rel expression in T cells, inhibiting interleukin-2 (IL-2) mRNA induction. This targeted molecular action suggests potential advantages for manipulating T cell responses in treating diseases.

Area of Science:

  • Immunology
  • Molecular Biology
  • Pharmacology

Background:

  • Pentoxifylline (PF), a methyl xanthine derivative, is gaining interest for treating T cell-dependent diseases.
  • Understanding the molecular effects of PF during lymphocyte activation is crucial for its clinical application.

Purpose of the Study:

  • To investigate the molecular consequences of pentoxifylline (PF) treatment on T lymphocyte activation.
  • To determine the specific transcription factors and genes affected by PF during T cell activation.

Main Methods:

  • Studied molecular changes in T cells upon anti-CD3 stimulation and PF treatment.
  • Analyzed the expression of NF-kappaB family members (c-Rel, NF-AT) and IL-2/IL-2R(alpha) mRNA.
  • Utilized transient transfection experiments to confirm the role of c-Rel in IL-2 gene regulation.

Main Results:

  • PF blocked anti-CD3-induced c-Rel expression in T cells, but not other NF-kappaB members or NF-AT induction.
  • PF suppressed IL-2 mRNA induction while IL-2R(alpha) chain mRNA induction remained unaffected.
  • c-Rel was implicated as a key factor in IL-2 gene promotion.
  • PF did not block c-Rel induction in B cells, indicating cellular selectivity.

Conclusions:

  • Pentoxifylline exhibits selective inhibition of c-Rel expression and IL-2 mRNA induction in T cells.
  • The findings suggest c-Rel is a critical regulator of IL-2 gene expression.
  • PF's molecular and cellular selectivity may offer therapeutic advantages over other drugs like FK506 for T cell-mediated diseases.

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