Inhibition of the antigen activated T cell response by methylprednisolone is caused by inhibition of interleukin-2 (IL-2) production.
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.
D000941:Antigens / Q000276:immunology; D002455:Cell Division / Q000187:drug effects; D006801:Humans; D066298:In Vitro Techniques; D007376:Interleukin-2 / Q000096:biosynthesis*; D008775:Methylprednisolone / Q000494:pharmacology*; D009000:Monocytes / Q000276:immunology; D013601:T-Lymphocytes / Q000187:drug effects* / Q000276:immunology
D000941:Antigens; D007376:Interleukin-2; D008775:Methylprednisolone