Interleukin-2 can prevent and reverse antigen-induced unresponsiveness in cloned human T lymphocytes

Immunology. 1988 Jul;64(3):413-7.

Abstract

The exposure of human T-cell clones to supra-immunogenic concentrations of peptide antigen in the absence of accessory cells induces antigen-specific unresponsiveness. Using this model we have investigated the ability of cytokines to modulate the induction of, or reversal of, T-cell tolerance. Our findings demonstrate that interleukin-2 (IL-2), but not interferon-gamma (IFN-gamma) or interleukin-1 (IL-1), is able to inhibit the induction of T-cell unresponsiveness in a dose-dependent fashion. Moreover, IL-2 was able to reverse established antigen-dependent T-cell unresponsiveness. In order to determine if modulation of IL-2 receptors is able to induce or abrogate unresponsiveness, the T cells were treated with anti-Tac antibody alone or together with tolerizing concentrations of antigen. Anti-Tac antibody was neither able to induce nor inhibit the induction of tolerance. The application of this model in the manipulation of immune responses is discussed here.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens / immunology
  • Clone Cells / immunology
  • Epitopes / immunology
  • Humans
  • Immune Tolerance*
  • Interferon-gamma / pharmacology
  • Interleukin-1 / pharmacology
  • Interleukin-2 / pharmacology*
  • Peptides / immunology
  • Receptors, Immunologic / immunology
  • Receptors, Interleukin-2
  • T-Lymphocytes / immunology*

Substances

  • Antigens
  • Epitopes
  • Interleukin-1
  • Interleukin-2
  • Peptides
  • Receptors, Immunologic
  • Receptors, Interleukin-2
  • Interferon-gamma