Class IIa HDAC4 and HDAC7 Cooperatively Regulate Gene Transcription in Th17 Cell Differentiation

    April 2024 in “ Proceedings of the National Academy of Sciences ”
    Ka Lung Cheung, Li Zhao, Rajal Sharma, Anurupa Ghosh, Michael G. Appiah, Yifei Sun, Anbalagan Jaganathan, Yuan Hu, Alannah Lejeune, Feihong Xu, Xinye Han, Xueting Wang, Fan Zhang, Chunyan Ren, Martin J. Walsh, Huabao Xiong, Alexander M. Tsankov, Ming‐Ming Zhou
    TLDR HDAC4 and HDAC7 are crucial for Th17 cell development and could be targeted to treat inflammatory diseases.
    This study investigates the role of class IIa histone deacetylases, HDAC4 and HDAC7, in the differentiation of mouse T-helper 17 (Th17) cells from naive CD4<sup>+</sup> T cells. HDAC4 and HDAC7 are shown to be selectively induced and functionally important in Th17 cell differentiation, but not in other T-helper subtypes. HDAC4 interacts with the transcription factor JunB to activate Th17 signature genes, while HDAC7 collaborates with Aiolos and Smrt/Ncor1-Hdac3 corepressors to repress negative regulators of Th17 differentiation. Inhibition of HDAC4/7 reduces Th17 cell-mediated intestinal inflammation in a colitis mouse model, suggesting that targeting these enzymes could be a therapeutic strategy for Th17-related inflammatory diseases like ulcerative colitis.
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