Maisonneuve-Rosemont Hospital Research Center, Montréal, Québec, Canada.
Département de microbiologie, infectiologie et immunologie, Université de Montréal, Montréal, Québec, Canada.
PLoS One. 2019 Apr 5;14(4):e0215012. doi: 10.1371/journal.pone.0215012. eCollection 2019.
During CD8+ T cell response, Notch signaling controls short-lived-effector-cell (SLEC) generation, but the exact mechanisms by which it does so remains unclear. The Notch signaling pathway can act as a key regulator of Akt signaling via direct transcriptional induction of Hes1, which will then repress the transcription of Pten, an inhibitor of Akt signaling. As both Notch and Akt signaling can promote effector CD8+ T cell differentiation, we asked whether Notch signaling influences SLEC differentiation via the HES1-PTEN axis. Here, we demonstrate that HES1 deficiency in murine CD8+ T cells did not impact SLEC differentiation. Moreover, we show that Pten transcriptional repression in effector CD8+ T cells is not mediated by Notch signaling although Akt activation requires Notch signaling. Therefore, HES1 is not an effector of Notch signaling during CD8+ T cell response.
在 CD8+ T 细胞反应期间，Notch 信号通路控制着短暂效应细胞（SLEC）的产生，但 Notch 信号通路具体是如何做到这一点的仍不清楚。Notch 信号通路可以通过直接转录诱导 Hes1 作为 Akt 信号的关键调节剂，从而抑制 Akt 信号抑制剂 Pten 的转录。由于 Notch 和 Akt 信号都可以促进效应 CD8+ T 细胞的分化，我们想知道 Notch 信号是否通过 HES1-PTEN 轴影响 SLEC 的分化。在这里，我们证明了小鼠 CD8+ T 细胞中 Hes1 的缺失并不影响 SLEC 的分化。此外，我们还表明，效应 CD8+ T 细胞中 Pten 的转录抑制不是由 Notch 信号介导的，尽管 Akt 的激活需要 Notch 信号。因此，在 CD8+ T 细胞反应中，HES1 不是 Notch 信号的效应物。
