Cited by 140T-cell and B-cell ImmunologyPsoriasis: Treatment and PathogenesisFOXO transcription factor regulation

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Inflammation negatively regulates FOXP3 and regulatory T-cell function via DBC1

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Gao, Yayi, Tang, Jiayou, Chen, Weiqian, Li, Qiang, Nie, Jia, Lin, Fang, Wu, Qingsi, Chen, Zuojia, Gao, Zhimei, Fan, Huimin, Tsun, Andy, Shen, Jijia, Chen, Guihua, Liu, Zhongmin, Lou, Zhenkun, Olsen, Nancy J., Zheng, Song Guo, Li, Bin·2015·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.1421463112PMC PMC4485127

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Abstract

Significance: Treg cells suppress excessive and aberrant immune responses. Impaired function or homeostasis of Treg cells would induce severe autoimmune and inflammatory diseases. Forkhead box P3 (FOXP3), as a master regulator of Treg cells, forms a large complex with other binding factors to modulate Treg-cell function subtly in pathological and physiological conditions. We identified that Deleted in breast cancer 1 (DBC1) is an essential subunit of the FOXP3 complex in human CD4 + Treg cells. Our results show that the inflammatory cytokines TNF-α or IL-6 trigger FOXP3 degradation, whereas downregulation of DBC1 expression prevents FOXP3 degradation and maintains Treg-cell function under inflammatory stimuli in vitro and in vivo. These findings unveil a previously unidentified pathway for therapeutically modulating FOXP3 + Treg-cell stability under inflammation.

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Self-citation

Authors: Gao, Y., Tang, J., Chen, W., Li, Q., Nie, J., Lin, F., Wu, Q., Chen, Z., Gao, Z., Fan, H., Tsun, A., Shen, J., Chen, G., Liu, Z., Lou, Z., Olsen, N. J., Zheng, S. G., & Li, B.
Affiliations: Sun Yat-sen University (CN)
Tongji University (CN)
Pennsylvania State University (US)
Chinese Academy of Sciences (CN)
Anhui Medical University (CN)
Mayo Clinic (US)
ORCID: Gao, Yayi
Tang, Jiayou
Chen, Weiqian
Li, Qiang
Nie, Jia
Chen, Zuojia
Fan, Huimin
Tsun, Andy
Chen, Guihua
Liu, Zhongmin
Lou, Zhenkun
Olsen, Nancy J.
Zheng, Song Guo
Li, Bin
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2015-06-09
Volume: 112
Issue: 25
Pages: E3246-54
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.1421463112
PMC: PMC4485127
OpenAlex: W1503625166
Cited by: 140
References: 43
Citations by year: 2026: 12 · 2025: 12 · 2024: 6 · 2023: 9 · 2022: 12 · 2021: 18 · 2020: 27 · 2019: 20 · 2018: 11 · 2017: 7 · 2016: 4 · 2015: 1
FWCI: 3.78
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.pnas.org/site/misc/userlicense.xhtml (vor, 183 d)
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: HHS | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR059103)
Topics: Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › FOXO transcription factor regulation
Keywords: Foxp3, regulatory T cells, DBC1, inflammation, protein stability, protein degradation, experimental autoimmune encephalomyelitis, colitis, immune homeostasis, inflammatory diseases
MeSH terms: Animals, Encephalomyelitis, Autoimmune, Experimental, Mice, Inbred C57BL, Adaptor Proteins, Signal Transducing, T-Lymphocytes, Regulatory, Mice, Forkhead Transcription Factors

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Inflammation negatively regulates FOXP3 and regulatory T-cell function via DBC1

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