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

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 f...

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Bibliographic Details
Main Authors: Essery, G, Feldmann, M, Lamb, JR
Format: Journal article
Language:English
Published: 1988
Description
Summary: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.