Ubiquitin-Dependent Regulation of Treg Function and Plasticity

被引:2
|
作者
Dong, Yi [1 ]
Pan, Fan [2 ]
机构
[1] Johns Hopkins Univ, Sch Med, Dept Cell Biol, Baltimore, MD USA
[2] Chinese Acad Sci, Shenzhen Inst Adv Technol, Ctr Canc Immunol Res, Shenzhen, Guangdong, Peoples R China
关键词
Treg; Ubiquitin; Posttranslational regulation; Foxp3; T-CELL DEVELOPMENT; TRANSCRIPTION FACTOR FOXP3; DE-NOVO DIFFERENTIATION; TGF-BETA; AUTOIMMUNE-DISEASE; SELF-TOLERANCE; CUTTING EDGE; CBL-B; LINEAR UBIQUITINATION; SUPPRESSIVE FUNCTION;
D O I
10.1007/978-981-15-6407-9_4
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
As an indispensable part of peripheral tolerance, regulatory T (Treg) cells play an important role in immune homeostasis by suppressing other immune cells. Behind this function is a complex network of transcription factors and signaling cascades that regulates the function and plasticity of regulatory T cells. Among these, Forkhead box P3 (Foxp3) is considered as the master transcription factor, and its stability will influence the function and viability of Treg cells. Because of this, understanding the mechanisms that regulate Foxp3 and its co-regulators will provide more understanding to Treg cells and uncover more targets to manipulate Treg cells in treating autoimmune diseases, organ transplantation, and tumor. Interestingly, several recent studies show that ubiquitin-dependent pathways are important regulators of Foxp3, which suggest both great scientific and therapeutic values. In this chapter, we cover emerging evidence of ubiquitin-dependent, posttranslational regulation of Treg function and plasticity.
引用
收藏
页码:63 / 80
页数:18
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