Department of Microbiology, New York University School of Medicine, Smilow Research Center, 522 First Avenue, Smilow Building Rm:1011, New York, New York 10016, USA.
Adv Exp Med Biol. 2009;665:47-59. doi: 10.1007/978-1-4419-1599-3_4.
The Transcription factor FoxP3 belongs to the forkhead/winged-helix family of transcriptional regulators and shares general structural features with other FoxP family members. FoxP3 functions as a master of transcription for the development of regulatory T-cells (Treg cells) both in humans and in mice. Natural genetic mutations ofFoxP3 that disrupt its function in humans result in an autoimmune syndrome called Immune Polyendocrinopathy, Enteropathy, X-linked (IPEX) and in mice, its deletion causes the Scurfy phenotype, with similar pathology. The finding that FoxP3 is required for the development and function of Tregs has led to an explosion of research in determining its regulation and function in the immune system. Understanding the biological properties of FoxP3 has a wide range of implications for immune tolerance, autoimmune disorders, inflammation and immune response to infectious diseases and cancer.
转录因子 FoxP3 属于叉头/翼状螺旋转录调控因子家族,与其他 FoxP 家族成员具有共同的结构特征。FoxP3 作为人类和小鼠调节性 T 细胞(Treg 细胞)发育的转录主因子发挥作用。FoxP3 的天然基因突变使其在人类中的功能受到破坏,导致一种自身免疫综合征,称为免疫多内分泌腺病、肠病、X 连锁(IPEX),而在小鼠中,其缺失导致 Scurfy 表型,具有相似的病理学。发现 FoxP3 对于 Treg 的发育和功能是必需的,这导致了对其在免疫系统中的调控和功能的研究的爆发。理解 FoxP3 的生物学特性对于免疫耐受、自身免疫性疾病、炎症以及对传染病和癌症的免疫反应具有广泛的意义。