期刊
NATURE COMMUNICATIONS
卷 9, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-018-05676-6
关键词
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资金
- National Natural Science Foundation of China [31230037, 31670896, 31370904, 81671579, 91753141]
- Ministry of Science and Technology of China [2013CB910900]
- National Key Research and Development Program [2017YFA0104500]
- Recruitment Program of Global Experts of China
- Shanghai Rising-Star Program [16QA1403300]
- Shanghai Municipal Commission of Health and Family Planning [20174Y0049, 20174Y0191]
- Shanghai Jiao Tong University Program for young teachers [KJ30214170006]
- Medical and Engineering Cross Research Foundation [YG2016QN77]
Regulatory T (Treg) cells are essential for maintaining immune homeostasis and tolerance, but the mechanisms regulating the stability and function of Treg cells have not been fully elucidated. Here we show SUMO-specific protease 3 (SENP3) is a pivotal regulator of Treg cells that functions by controlling the SUMOylation and nuclear localization of BACH2. Treg cell-specific deletion of Senp3 results in T cell activation, autoimmune symptoms and enhanced antitumor T cell responses. SENP3-mediated BACH2 deSUMOylation prevents the nuclear export of BACH2, thereby repressing the genes associated with CD4+ T effector cell differentiation and stabilizing Treg cell-specific gene signatures. Notably, SENP3 accumulation triggered by reactive oxygen species (ROS) is involved in Treg cell-mediated tumor immunosuppression. Our results not only establish the role of SENP3 in the maintenance of Treg cell stability and function via BACH2 deSUMOylation but also clarify the function of SENP3 in the regulation of ROS-induced immune tolerance.
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