SELECTIVE UP-REGULATION BY INTERFERON-GAMMA OF SURFACE MOLECULES OF THE LY-6 COMPLEX IN RESTING T-CELLS - THE LY-6A/E AND TAP ANTIGENS ARE PREFERENTIALLY ENHANCED
SELECTIVE UP-REGULATION BY INTERFERON-GAMMA OF SURFACE MOLECULES OF THE LY-6 COMPLEX IN RESTING T-CELLS - THE LY-6A/E AND TAP ANTIGENS ARE PREFERENTIALLY ENHANCED
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DOI：
10.1002/eji.1830170816
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发表时间：
1987-08-01
影响因子：
5.4
通讯作者：
COKER, L
中科院分区：
文献类型：
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作者：
DUMONT, FJ;DIJKMANS, R;COKER, L
由小鼠Ly-6基因座编码的表面分子可以阻断T细胞中的触发信号，因此可能在T细胞功能中起重要作用。以前，我们发现Ly-6分子被干扰素（IFN）-α上调。β的在静止的T细胞中。在此，我们研究了IFN-γ的可能影响。在这些分子上。将来自C57 BL/6（Ly-6.2）和BALB/c（Ly-6.1）小鼠的纯化T细胞与重组鼠IFN-γ体外孵育。流式细胞术检测Ly-6抗原的表达。发现Ly-6A/E和T细胞活化蛋白（TAP）分子均显著增强，而Ly-6C受影响较小。在相同的条件下，其他T细胞表面分子显示没有或轻微的变化。IFN-γ的作用对Ly-6A/E和TAP表达的抑制作用在低至10 U/ml时达到最大，并且仅需要18-24 h的温育。此外，由IFN-γ诱导的Ly-6A表达的增强也可被抑制。至少稳定5天。T细胞亚群的分析进一步揭示了IFN-γ- Ly-6A（C57 BL/6小鼠）的诱导增加涉及Lyt-2+和L3 T4+细胞，而Ly-6 E（BALB/c小鼠）的增加在Lyt-2+细胞中更明显。这些表型改变的功能后果进行了评估，通过研究有丝分裂反应的T细胞抗体介导的赖氨酸-6交联的佛波醇肉豆蔻酸酯乙酸酯的存在下。用IFN-γ预处理静息T细胞显著增加了对抗Ly-6A和抗Ly-6 E单克隆抗体的应答。IFN-.gamma.当这种刺激在次优条件下进行时，处理还增强了由抗TAP单克隆抗体诱导的刺激。因此，IFN-γ。选择性上调静息T细胞中的Ly-6A/E和TAP活化途径。我们推测这种作用可能有助于IFN-γ的免疫调节活性。
Surface molecules encoded by the murine Ly-6 locus can transduce triggering signals in T cells and thus may play important roles in T cell function. Previously, we found that Ly-6 molecules are up-regulated by interferon (IFN)-.alpha./.beta. in resting T cells. Here, we examined the possible influence of IFN-.gamma. on these molecules. Purified T cells from C57BL/6 (Ly-6.2) and BALB/c (Ly-6.1) mice were incubated in vitro with recombinant murine IFN-.gamma. and the expression of Ly-6 antigens was measured by flow cytofluorometry. It was found that both Ly-6A/E and T cell-activating protein (TAP) molecules are markedly enhanced while Ly-6C is less affected. Under the same conditions, other T cell surface molecules showed no or marginal changes. The effect of IFN-.gamma. on Ly-6A/E and TAP expression reached a maximum with as little as 10 U/ml and required only 18-24 h of incubation. Moreover, the enhancement of Ly-6A expression induced by IFN-.gamma. was stable for at least 5 days. Analysis of T cell subsets further revealed that IFN-.gamma.-induced augmentation of Ly-6A (C57BL/6 mice) involves both Lyt-2+ and L3T4+ cells while the increase of Ly-6E (BALB/c mice) is more pronounced in Lyt-2+ cells. The functional consequence of these phenotypic alterations was evaluated by studying the mitogenic responses of T cells to antibody-mediated Ly-6 cross-linking in the presence of phorbol myristate acetate. Pretreatment of resting T cells with IFN-.gamma. dramatically increased the responses to anti-Ly-6A and anti-Ly-6E monoclonal antibodies. IFN-.gamma. treatment also boosted the stimulation induced by anti-TAP monoclonal antibody when this stimulation was performed under suboptimal conditions. Therefore, IFN-.gamma. selectively up-regulates the Ly-6A/E and TAP activation pathways in resting T cells. We speculate that this effect may contribute to the immunoregulatory activities of IFN-.gamma.