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首页> 外文期刊>Cell Reports >Id3 Maintains Foxp3 Expression in Regulatory T Cells by Controlling a Transcriptional Network of E47, Spi-B, and SOCS3
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Id3 Maintains Foxp3 Expression in Regulatory T Cells by Controlling a Transcriptional Network of E47, Spi-B, and SOCS3

机译：Id3通过控制E47，Spi-B和SOCS3的转录网络来维持调节性T细胞中Foxp3的表达。

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The transcription factor Foxp3 dominantly controls regulatory T (Treg) cell function, and only its continuous expression guarantees the maintenance of full Treg cell-suppressive capacity. However, transcriptional regulators maintaining Foxp3 transcription are incompletely described. Here, we report that high E47 transcription factor activity in Treg cells resulted in unstable Foxp3 expression. Under homeostatic conditions, Treg cells expressed high levels of the E47 antagonist Id3, thus restricting E47 activity and maintaining Foxp3 expression. In contrast, stimulation of Id3-deficient or E47-overexpressing Treg cells resulted in the loss of Foxp3 expression in a subset of Treg cells in vivo and in vitro. Mechanistic analysis indicated that E47 activated expression of the transcription factor Spi-B and the suppressor of cytokine signaling 3 (SOCS3), which both downregulated Foxp3 expression. These findings demonstrate that the balance of Id3 and E47 controls the maintenance of Foxp3 expression in Treg cells and, thus, contributes to Treg cell plasticity.
机译：转录因子Foxp3主要控制调节性T（Treg）细胞功能，只有连续表达才能保证维持完整的Treg细胞抑制能力。但是，保持Foxp3转录的转录调节子不完整地描述。在这里，我们报告在Treg细胞中高E47转录因子活性导致不稳定的Foxp3表达。在稳态条件下，Treg细胞表达高水平的E47拮抗剂Id3，从而限制E47活性并维持Foxp3表达。相反，在体内和体外刺激Id3缺失或E47过度表达的Treg细胞导致Foxp3表达丧失。机理分析表明，E47激活转录因子Spi-B的表达和细胞因子信号传导3（SOCS3）的抑制剂，两者均下调Foxp3的表达。这些发现表明，Id3和E47的平衡控制着Treg细胞中Foxp3表达的维持，因此有助于Treg细胞的可塑性。

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