Immune regulation by histone deacetylases: a focus on the alteration of FOXP3 activity

被引:34
|
作者
Zhang, Hongtao [1 ]
Xiao, Yan [1 ]
Zhu, Zhiqiang [1 ]
Li, Bin [2 ]
Greene, Mark I. [1 ]
机构
[1] Univ Penn, Dept Pathol & Lab Med, Perelman Sch Med, Philadelphia, PA 19104 USA
[2] Inst Pasteur Shanghai, Unit Mol Immunol, Key Lab Mol Virol & Immunol, Shanghai, Peoples R China
来源
IMMUNOLOGY AND CELL BIOLOGY | 2012年 / 90卷 / 01期
基金
美国国家卫生研究院;
关键词
FOXP3; acetylation; HDAC; HAT; Treg cells; T-CELL FUNCTION; AUTOIMMUNE-DISEASE; PROMOTER OCCUPANCY; GENE-EXPRESSION; NUCLEAR EXPORT; IN-VIVO; ACETYLATION; PROTEIN; INHIBITION; BINDING;
D O I
10.1038/icb.2011.101
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Several histone deacetylases (HDACs) are involved in the regulation of forkhead box protein P3 (FOXP3) expression and function by affecting features of FOXP3 protein stability. FOXP3, a forkhead family transcription factor specially expressed in regulatory T (Treg) cells, controls the expression of many key immune-regulatory genes. Treg cells are a population of T lymphocytes that have critical roles in the immune system homeostasis and tolerance to self and foreign antigens, the body's response to cancer and infectious agents. FOXP3 forms oligomeric complexes with other proteins, the components of which are believed to be regulated dynamically. In addition, HDAC activities influence FOXP3 interactions with other partners to form transcriptional regulatory complexes. By understanding the details of the biochemical and structural basis of the regulation of FOXP3 acetylation, therapeutic strategies for diseases related to Treg cells may emerge. Immunology and Cell Biology (2012) 90, 95-100; doi: 10.1038/icb.2011.101; published online 29 November 2011
引用
收藏
页码:95 / 100
页数:6
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