Avitahl N, Winandy S, Friedrich C, Jones B, Ge Y, Georgopoulos K
Cutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Charlestown 02129, USA.
Immunity. 1999 Mar;10(3):333-43. doi: 10.1016/s1074-7613(00)80033-3.
T cell activation involves the sustained accumulation of T cell receptor (TCR) and IL-2 receptor (IL-2R) mediated signaling events that promote cell cycle entry and progression. The Ikaros family of nuclear factors regulate this process by providing thresholds overcome by receptor signaling. T cells with reduced levels of Ikaros activity require fewer TCR engagement events for activation, exhibit a greater proliferative response to IL-2, and are less sensitive to inhibitors of TCR and IL-2R signaling. Upon T cell activation, Ikaros proteins localize in a higher-order chromatin structure where they colocalize with components of the DNA replication machinery. Proliferating T cells with reduced Ikaros activity display chromosome abnormalities. We propose that participation of Ikaros in higher-order chromatin structures controls cell cycle transitions and restricts DNA replication.
T细胞活化涉及T细胞受体(TCR)和白细胞介素-2受体(IL-2R)介导的信号事件的持续积累,这些信号事件促进细胞进入细胞周期并推动其进程。Ikaros家族核因子通过提供受体信号传导需克服的阈值来调节这一过程。Ikaros活性水平降低的T细胞激活所需的TCR结合事件更少,对IL-2表现出更强的增殖反应,并且对TCR和IL-2R信号传导抑制剂的敏感性更低。T细胞活化后,Ikaros蛋白定位于更高阶的染色质结构中,在那里它们与DNA复制机制的成分共定位。Ikaros活性降低的增殖T细胞表现出染色体异常。我们提出,Ikaros参与更高阶染色质结构控制细胞周期转换并限制DNA复制。