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首页> 外文期刊>Cellular immunology >CD4 co-receptor dependent signaling promotes competency for re-stimulation induced cell death of effector T cells.
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CD4 co-receptor dependent signaling promotes competency for re-stimulation induced cell death of effector T cells.

机译：CD4共受体依赖性信号传导增强了重新刺激效应T细胞诱导的细胞死亡的能力。

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摘要

The elimination of activated T cells by FAS-mediated signaling is an important immunoregulatory mechanism used to maintain homeostasis and prevent tissue damage. T cell receptor-dependent signals are required to confer sensitivity to FAS-mediated re-stimulation-induced cell death (RICD), however, the nature of these signals is not well understood. In this report, we show, using T cells from CD4-deficient mice reconstituted with a tail-less CD4 transgene, that CD4-dependent signaling events are a critical part of the competency signal required for RICD. This is in part due to defects in FAS receptor signaling complex formation as shown by decreased recruitment of FAS and caspase 8 into lipid rafts following antigen re-stimulation in the absence of CD4-dependent signals. In addition, in the absence of CD4-dependent signals, effector T cells have a selective defect in IL-2 secretion following peptide re-stimulation, while provision of exogenous IL-2 during re-stimulation partially restores susceptibility to RICD. Importantly, IL-2 production and proliferation after primary peptide stimulation is comparable between wild type and CD4-deficient T cells indicating that the requirement for CD4-dependent signaling events for IL-2 production is developmentally regulated and is particularly critical in previously activated effector T cells. In total, our results indicate that CD4 co-receptor dependent signaling events specifically regulate effector T cell survival and function. Further, these data suggest that CD4-dependent signaling events may protect against the decreased IL-2 production and resistance to cell death seen during chronic immune stimulation.
机译：通过FAS介导的信号消除活化T细胞是一种重要的免疫调节机制，可用于维持体内稳态和防止组织损伤。需要T细胞受体依赖性信号来赋予对FAS介导的再刺激诱导的细胞死亡（RICD）的敏感性，但是，这些信号的性质尚未得到很好的理解。在此报告中，我们显示，使用来自无尾CD4转基因重组的CD4缺陷小鼠的T细胞，CD4依赖性信号事件是RICD所需能力信号的关键部分。这部分归因于FAS受体信号复合物形成的缺陷，如在缺乏CD4依赖性信号的情况下，抗原重新刺激后FAS和caspase 8减少进入脂质筏所显示的。另外，在缺乏CD4依赖性信号的情况下，效应T细胞在肽重新刺激后IL-2分泌中具有选择性缺陷，而在重新刺激过程中提供外源IL-2部分恢复了对RICD的敏感性。重要的是，一级肽刺激后，IL-2的产生和增殖在野生型和CD4缺陷型T细胞之间是可比的，这表明IL-2产生对CD4依赖性信号转导事件的需求受到发育调节，并且在先前激活的效应子T中尤其重要细胞。总的来说，我们的结果表明CD4受体依赖的信号转导事件特异性调节效应T细胞的存活和功能。此外，这些数据表明，依赖CD4的信号转导事件可以预防在慢性免疫刺激过程中IL-2产生的减少和对细胞死亡的抵抗。

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