SENP3 maintains the stability and function of regulatory T cells via BACH2 deSUMOylation

Xiaoyan Yu, Yimin Lao, Xiao-Lu Teng, Song Li, Yan Zhou, Feixiang Wang, Xinwei Guo, Siyu Deng, Yuzhou Chang, Xuefeng Wu, Zhiduo Liu, Lei Chen, Li-Ming Lu, Jinke Cheng, Bin Li, Bing Su, Jin Jiang, Hua-Bing Li (), Chuanxin Huang (), Jing Yi () and Qiang Zou ()
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Xiaoyan Yu: Shanghai Jiao Tong University School of Medicine
Yimin Lao: Shanghai Jiao Tong University School of Medicine
Xiao-Lu Teng: Shanghai Jiao Tong University School of Medicine
Song Li: Shanghai Jiao Tong University School of Medicine
Yan Zhou: Shanghai Jiao Tong University School of Medicine
Feixiang Wang: Shanghai Jiao Tong University School of Medicine
Xinwei Guo: Shanghai Jiao Tong University School of Medicine
Siyu Deng: Shanghai Jiao Tong University School of Medicine
Yuzhou Chang: Shanghai Jiao Tong University School of Medicine
Xuefeng Wu: Shanghai Jiao Tong University School of Medicine
Zhiduo Liu: Shanghai Jiao Tong University School of Medicine
Lei Chen: Shanghai Jiao Tong University School of Medicine
Li-Ming Lu: Shanghai Jiao Tong University School of Medicine
Jinke Cheng: Shanghai Jiao Tong University School of Medicine
Bin Li: Shanghai Jiao Tong University School of Medicine
Bing Su: Shanghai Jiao Tong University School of Medicine
Jin Jiang: University of Texas Southwestern Medical Center
Hua-Bing Li: Shanghai Jiao Tong University School of Medicine
Chuanxin Huang: Shanghai Jiao Tong University School of Medicine
Jing Yi: Shanghai Jiao Tong University School of Medicine
Qiang Zou: Shanghai Jiao Tong University School of Medicine

Nature Communications, 2018, vol. 9, issue 1, 1-11

Abstract: Abstract 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.

Date: 2018
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DOI: 10.1038/s41467-018-05676-6

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