Yamada Takeshi, Gierach Kirsten, Lee Ping-Hsien, Wang Xiaohong, Lacorazza H Daniel
Department of Pathology and Immunology, Baylor College of Medicine, Houston, TX 77030, USA.
J Immunol. 2010 Oct 1;185(7):3824-8. doi: 10.4049/jimmunol.1000718. Epub 2010 Aug 27.
T cell receptor activation inhibits expression of the E74-like factor (ELF) 4 and Krüppel-like factor 4 genes to release naive CD8(+) T cells from their quiescent state. In this study, we show that ELF4 controls the ERK-mediated proliferative response by maintaining normal levels of dual-specificity phosphatases 1 and 5 in CD8(+) T cells. In activated CD8(+) T cells, the mammalian target of rapamycin pathway inhibits ELF4 and Krüppel-like factor 4 expression downstream of ERK and PI3K signaling. Our findings demonstrate that rapamycin could be used to modulate expression of this transcriptional network involved in cell-cycle regulation.
T细胞受体激活可抑制E74样因子（ELF）4和Krüppel样因子4基因的表达，从而使初始CD8(+) T细胞从静止状态中释放出来。在本研究中，我们发现ELF4通过维持CD8(+) T细胞中双特异性磷酸酶1和5的正常水平来控制ERK介导的增殖反应。在活化的CD8(+) T细胞中，雷帕霉素靶蛋白通路在ERK和PI3K信号传导的下游抑制ELF4和Krüppel样因子4的表达。我们的研究结果表明，雷帕霉素可用于调节参与细胞周期调控的这一转录网络的表达。
