Differential inhibition of the T cell activation pathway by dexamethasone and cyclosporine

Transplantation. 1990 Mar;49(3):560-4. doi: 10.1097/00007890-199003000-00017.

Abstract

We examined the inhibitory capacity of dexamethasone (DEX) and cyclosporine (CsA) on T cell activation using various accessory cell (AC)-dependent and AC-independent stimuli. We found that CsA strongly inhibited T cell activation in each of the assays used: allogeneic T cell stimulation, phorbol myristate acetate plus concanavalin A, PMA plus anti-CD3 monoclonal antibody (2C11), or PMA plus ionomycin (IONO) T cell activation. DEX was a potent inhibitor of allogeneic stimulation and of the PMA+Con A- or PMA + 2C11-induced T cell stimulation. PMA + IONO stimulation, however, was not affected by DEX. When inhibition occurred, both drugs suppressed [3H]TdR incorporation, IL-2 production, and IL-2 mRNA accumulation, indicating that the sites of interference of these drugs in the T cell activation pathway are located proximal to IL-2 mRNA accumulation. However, the difference in the effects of DEX and CsA in PMA + IONO stimulation suggests that DEX and CsA differentially affect T cell activation.

MeSH terms

  • Animals
  • Antigen-Presenting Cells / immunology
  • Cyclosporins / pharmacology*
  • Dexamethasone / pharmacology*
  • Gene Expression / drug effects
  • Interleukin-2 / biosynthesis
  • Interleukin-2 / genetics
  • Ionomycin / pharmacology
  • Leukotriene B4 / pharmacology
  • Lymphocyte Activation / drug effects*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C3H
  • RNA, Messenger / genetics
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology*
  • Tetradecanoylphorbol Acetate / pharmacology

Substances

  • Cyclosporins
  • Interleukin-2
  • RNA, Messenger
  • Leukotriene B4
  • Ionomycin
  • Dexamethasone
  • Tetradecanoylphorbol Acetate