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

@article{Gao2015InflammationNR,
  title={Inflammation negatively regulates FOXP3 and regulatory T-cell function via DBC1.},
  author={Yayi Gao and Jiayou Tang and Weiqian Chen and Qiang Li and Jia Nie and Fang Lin and Qingsi Wu and Zuojia Chen and Zhimei Gao and Huimin Fan and Andy Tsun and Jijia Shen and Guihua Chen and Zhongmin Liu and Zhenkun Lou and Nancy J Olsen and Song Guo Zheng and Bin Li},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2015},
  volume={112 25},
  pages={E3246-54}
}
Forkhead box P3 (FOXP3)-positive Treg cells are crucial for maintaining immune homeostasis. FOXP3 cooperates with its binding partners to elicit Treg cells' signature and function, but the molecular mechanisms underlying the modulation of the FOXP3 complex remain unclear. Here we report that Deleted in breast cancer 1 (DBC1) is a key subunit of the FOXP3 complex. We found that DBC1 interacts physically with FOXP3, and depletion of DBC1 attenuates FOXP3 degradation in inflammatory conditions… CONTINUE READING
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Critical role of all-trans retinoic acid in stabilizing human natural regulatory T cells under inflammatory conditions

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