Inhibition of the antigen activated T cell response by methylprednisolone is caused by inhibition of interleukin-2 (IL-2) production

Int J Immunopharmacol. 1984;6(5):419-23. doi: 10.1016/0192-0561(84)90079-1.

Abstract

A mechanism by which the steroid methylprednisolone inhibits the T cell proliferation normally seen in antigen driven cultures was investigated. At methylprednisolone concentrations less than 10 micrograms ml-1 inhibition of cellular proliferation was almost exclusively via the inhibition of the production of interleukin-2 by activated T cells. The steroid seemed to inhibit IL-2 production directly and not via reduced sensitivity to interleukin-1 by IL-2 producer T cells, or reduced IL-1 production by the antigen presenting monocytes. At methylprednisolone concentrations of greater than 10 micrograms ml-1 direct inhibition of the T cell receptor to antigen complexes presented by cooperating monocytes seemed the most likely explanation. T cells in the presence of antigen and monocytes and MP concentrations of greater than 10 micrograms ml-1 did not produce IL-2 and were incapable of expressing IL-2 receptors. The inhibiting effects of methylprednisolone therefore are via several mechanisms depending on the concentration of the steroid employed.

MeSH terms

  • Antigens / immunology
  • Cell Division / drug effects
  • Humans
  • In Vitro Techniques
  • Interleukin-2 / biosynthesis*
  • Methylprednisolone / pharmacology*
  • Monocytes / immunology
  • T-Lymphocytes / drug effects*
  • T-Lymphocytes / immunology

Substances

  • Antigens
  • Interleukin-2
  • Methylprednisolone