Nature Communications (Nov 2016)
USP21 prevents the generation of T-helper-1-like Treg cells
- Yangyang Li,
- Yue Lu,
- Shuaiwei Wang,
- Zhijun Han,
- Fuxiang Zhu,
- Yingmeng Ni,
- Rui Liang,
- Yan Zhang,
- Qibin Leng,
- Gang Wei,
- Guochao Shi,
- Ruihong Zhu,
- Dan Li,
- Haikun Wang,
- Song Guo Zheng,
- Hongxi Xu,
- Andy Tsun,
- Bin Li
Affiliations
- Yangyang Li
- Key Laboratory of Molecular Virology and Immunology, CAS Center for Excellence in Molecular Cell Science, Unit of Molecular Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Yue Lu
- School of Pharmacy, Shanghai University of Traditional Chinese Medicine
- Shuaiwei Wang
- Key Laboratory of Molecular Virology and Immunology, CAS Center for Excellence in Molecular Cell Science, Unit of Molecular Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Zhijun Han
- Chinese Academy of Sciences-Max Planck Society (MPG) Partner Institute for Computational Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Fuxiang Zhu
- Key Laboratory of Molecular Virology and Immunology, CAS Center for Excellence in Molecular Cell Science, Unit of Molecular Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Yingmeng Ni
- Department of Pulmonary Medicine, Rui Jin Hospital, School of Medicine, Shanghai Jiao Tong University
- Rui Liang
- Key Laboratory of Molecular Virology and Immunology, CAS Center for Excellence in Molecular Cell Science, Unit of Molecular Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Yan Zhang
- Key Laboratory of Molecular Virology and Immunology, Unit of Hematopoietic Stem Cell and Transgenic Animal Model, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Qibin Leng
- Key Laboratory of Molecular Virology and Immunology, Unit of Immune Regulation, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Gang Wei
- Chinese Academy of Sciences-Max Planck Society (MPG) Partner Institute for Computational Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Guochao Shi
- Department of Pulmonary Medicine, Rui Jin Hospital, School of Medicine, Shanghai Jiao Tong University
- Ruihong Zhu
- Flow Cytometry Core Facility, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Dan Li
- Key Laboratory of Molecular Virology and Immunology, CAS Center for Excellence in Molecular Cell Science, Unit of Molecular Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Haikun Wang
- Key Laboratory of Molecular Virology and Immunology, Unit of the Regulation of Immune Cell Differentiation, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Song Guo Zheng
- Clinical Immunology Center, Third Affiliated Hospital at Sun Yat-Sen University
- Hongxi Xu
- School of Pharmacy, Shanghai University of Traditional Chinese Medicine
- Andy Tsun
- Key Laboratory of Molecular Virology and Immunology, CAS Center for Excellence in Molecular Cell Science, Unit of Molecular Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Bin Li
- Key Laboratory of Molecular Virology and Immunology, CAS Center for Excellence in Molecular Cell Science, Unit of Molecular Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- DOI
- https://doi.org/10.1038/ncomms13559
- Journal volume & issue
-
Vol. 7,
no. 1
pp. 1 – 10
Abstract
The immunosuppressive role of regulatory T (Treg) cells largely depends on their virtue of expressing the transcription factor FOXP3. Here the authors show that the E3 deubiquitinase USP21 stabilizes FOXP3 by mediating its deubiquitination and helps to maintain the expression of Treg signature genes and Treg lineage stability in mice.
