Evidence that rapamycin inhibits interleukin-12-induced proliferation of activated T lymphocytes

Transplantation. 1994 Nov 27;58(10):1091-6.

Abstract

Interleukin 12 is a heterodimeric cytokine involved in the regulation of natural killer cell and T lymphocyte responses. In previous studies, we found that IL-12 induces proliferation of T cells only after co-stimulation with lectin, alloantigen, or anti-CD3 antibody. The IL-2-mediated proliferation of long-term T cell lines generated in this fashion is typically insensitive to the immunosuppressive agent, cyclosporine but sensitive to rapamycin. In this study, we examined the effect of cyclosporine and rapamycin on T cells responsive to IL-12. For long-term cultured T cell lines stimulated with phytohemagglutinin, alloantigen, or solid-phase anti-CD3 antibody, rapamycin blocked IL-12-induced proliferation to background levels. Culture in cyclosporine produced minimal inhibition of IL-12-induced T cell proliferation. Freshly isolated CD3+ cells did not proliferate in response to IL-12, nor did culture of these cells in IL-12 lead to upregulation of IL-2 receptor. These data suggest that the effect of IL-12, an important growth regulator for activated T lymphocytes, may involve late cellular activation events.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Antibodies
  • Binding, Competitive / drug effects
  • CD3 Complex / immunology
  • Cells, Cultured
  • Humans
  • Interleukin-12 / antagonists & inhibitors*
  • Lymphocyte Activation / drug effects*
  • Polyenes / pharmacology*
  • Receptors, Interleukin-2 / analysis
  • Sirolimus
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / ultrastructure
  • Time Factors

Substances

  • Antibodies
  • CD3 Complex
  • Polyenes
  • Receptors, Interleukin-2
  • Interleukin-12
  • Sirolimus