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抗原驱动的耐受后,人辅助性T细胞克隆对白细胞介素2的分泌有选择性抑制作用,但对干扰素-γ、肿瘤坏死因子-α或粒细胞/巨噬细胞集落刺激因子的分泌无抑制作用。

Selective inhibition of interleukin 2 but not of interferon-gamma, tumour necrosis factor-alpha or granulocyte/macrophage colony stimulating factor secretion by human helper T cell clones after antigen-driven tolerisation.

作者信息

Pawelec G, Sayers T, Busch F W

机构信息

Immunology Laboratory, Medical Clinic, University of Tübingen, F.R.G.

出版信息

Immunol Lett. 1989 Feb;20(3):187-91. doi: 10.1016/0165-2478(89)90078-3.

Abstract

Alloreactive human T-helper cell clones chronically exposed to specific antigen can become tolerised, i.e. lose their autocrine proliferative capacity and no longer undergo antigen-driven clonal expansion. To study parameters of possible clonal anergy in such cells, lymphokine secretion before and after tolerisation was measured. 10/10 CD4+ clones were found to secrete interleukin 2 (IL-2), interferon gamma, tumour necrosis factor alpha and granulocyte/macrophages colony stimulating factors. Tolerised clones which had lost autocrine proliferative capacity and had lost the ability to secret IL-2 nevertheless retained the ability to secrete the other lymphokines. These results thus show a highly selective lesion in the noncoordinate regulation of lymphokine secretion by tolerised cells.

摘要

长期暴露于特定抗原的同种异体反应性人类辅助性T细胞克隆可被耐受,即失去其自分泌增殖能力,不再经历抗原驱动的克隆扩增。为了研究此类细胞中可能的克隆无能参数,测量了耐受前后的淋巴因子分泌情况。发现10/10的CD4 +克隆可分泌白细胞介素2(IL-2)、γ干扰素、肿瘤坏死因子α和粒细胞/巨噬细胞集落刺激因子。失去自分泌增殖能力且失去分泌IL-2能力的耐受克隆仍保留分泌其他淋巴因子的能力。因此,这些结果显示了耐受细胞在淋巴因子分泌的非协同调节中存在高度选择性损伤。

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