Many aspects remain elusive of the mechanisms governing T cell quiescence. Here we show that E protein activity helps to establish a quiescent program in naïve T cells. Decreased E protein activity, as the consequence of enforced expression of an Id1 transgene, led to the accumulation of CD4+CD44hi T cells. The naïve CD4+ T cells from this transgenic strain mounted a vigorous proliferative response upon TCR stimulation, as a result of direct inhibition of E protein activity. Transcriptome analyses demonstrated that Id1-tg naïve CD4+ T cells exhibited a transcriptional profile characteristic of activated CD4+ T cells, with particular enrichment in the gene set related to PI3K-AKT signaling. Western blot analysis confirmed low but constitutive activation of this pathway. Moreover, the Id1-tg CD4+ T cells displayed enhanced formation of TCR microcluster. Taken together, these data support that downregulation of E protein activity facilitates the exit of naïve T cells from quiescence.

中文翻译：

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抑制E蛋白活性可通过调节PI3K-AKT信号传导和TCR微簇形成，促进幼稚CD4 + T细胞的静止退出。

许多方面仍然不清楚控制T细胞静止的机制。在这里，我们证明E蛋白的活性有助于在幼稚的T细胞中建立一个静止的程序。由于Id1转基因表达增强，导致E蛋白活性降低，导致CD4 + CD44hi T细胞积聚。由于直接抑制E蛋白活性，来自该转基因菌株的幼稚CD4 + T细胞在TCR刺激后产生了强烈的增殖反应。转录组分析表明，Id1-tg幼稚的CD4 + T细胞表现出活化CD4 + T细胞的转录特征，特别是在与PI3K-AKT信号相关的基因组中富集。蛋白质印迹分析证实了该途径的低水平但组成性活化。此外，Id1-tg CD4 + T细胞显示出增强的TCR微簇形成。综上所述，这些数据支持E蛋白活性的下调促进了幼稚T细胞从静止状态退出。