摘要
Foxp3,叉头/翼状螺旋转录因子3,是调节性T细胞发挥免疫抑制功能的关键性的转录因子。Foxp3与自身免疫性疾病,感染和肿瘤免疫逃避/逃逸的机制密切相关。参与Foxp3转录的主要信号通路包括:白细胞介素2受体(IL-2R)信号转导和转录激活因子(STAT)途径、转化生长因子β(TGF-β)/Smad通路、Notch信号通路、干扰素(IFN)/干扰素调节因子(IRF)和IFN/一氧化氮(NO)轴、磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(Akt)/哺乳动物雷帕霉素靶(mTOR)轴等。本文将对Foxp3的转录调控的分子机制进行归纳总结,旨在阐明其在自身免疫性疾病、炎性疾病、移植排斥、感染和肿瘤中所起的作用及机制。
Foxp3, forkhead/winged helix transcription factor 3, is a master transcription factor for the development and function of regulatory T cells. Foxp3 has been found to be associated with autoimmune diseases, infections, and tumor immune evasion/escape. The major signaling pathways regulating Foxp3 transcription include interleukin--2 receptor (IL -2R)/signal transducers and activators of transcription (STAT) pathway, the transforming growth factor--j3 (TOF-- beta)/Smad pathway, the Notch signaling pathway, the interferon (IFN)/IFN regulatory factor (IRF) axis and the IFN/ nitric oxide axis, and the phosphatidylinositol 3--kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (roTOR) axis. This article reviews the molecular mechanisms of transcriptional regulation by Foxp3 in order to reveal the action of this gene and its role in autoimmune diseases, inflammatory diseases, graft rejection, infections, and tumors.
出处
《中国病原生物学杂志》
CSCD
北大核心
2016年第5期I0003-I0004,F0003,F0004,共4页
Journal of Pathogen Biology
基金
国家自然科学基金项目(No.81401683)
江苏省自然科学基金项目(No.BK20140435)
江苏高校优势学科建设工程资助项目(PAPD)
南通大学博士启动基金项目(No.14B36)