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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.

Type

Journal article

Journal

Immunology

Publication Date

07/1988

Volume

64

Pages

413 - 417

Addresses

Charing Cross Sunley Research Centre, Hammersmith, London, U.K.

Keywords

T-Lymphocytes, Clone Cells, Humans, Peptides, Receptors, Immunologic, Receptors, Interleukin-2, Interleukin-1, Interleukin-2, Antigens, Epitopes, Immune Tolerance, Interferon-gamma