mTORC2型
PI3K/AKT/mTOR通路
mTORC1型
细胞生物学
蛋白激酶B
转录因子
细胞分化
化学
癌症研究
免疫系统
细胞内
信号转导
生物
免疫学
基因
生物化学
作者
Shigenori Nagai,Yutaka Kurebayashi,Shigeo Koyasu
摘要
Interleukin (IL)‐17–producing helper T (Th17) cells serve as a Th subset involved in epithelial cell– and neutrophil‐mediated immune responses against extracellular microbes and in the development of various autoimmune diseases. The differentiation of Th17 cells is controlled by a number of intracellular signaling cascades and a complex network of transcription factors. Recently, it has been shown that PI3K, Akt, and mammalian target of rapamycin (mTOR) complexes, such as mTORC1 and mTORC2, also positively regulate Th17 differentiation both in vivo and in vitro via multiple mechanisms; here, we review the current knowledge regarding the mechanisms through which these molecules enhance Th17 differentiation.
科研通智能强力驱动
Strongly Powered by AbleSci AI