Essery G, Feldmann M, Lamb J R
Charing Cross Sunley Research Centre, Hammersmith, London, U.K.
Immunology. 1988 Jul;64(3):413-7.
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.
在没有辅助细胞的情况下，将人类T细胞克隆暴露于超免疫原性浓度的肽抗原会诱导抗原特异性无反应性。利用该模型，我们研究了细胞因子调节T细胞耐受性诱导或逆转的能力。我们的研究结果表明，白细胞介素-2（IL-2）能够以剂量依赖的方式抑制T细胞无反应性的诱导，而干扰素-γ（IFN-γ）或白细胞介素-1（IL-1）则不能。此外，IL-2能够逆转已建立的抗原依赖性T细胞无反应性。为了确定IL-2受体的调节是否能够诱导或消除无反应性，单独用抗Tac抗体或与耐受浓度的抗原一起处理T细胞。抗Tac抗体既不能诱导也不能抑制耐受性的诱导。本文讨论了该模型在免疫反应操纵中的应用。
