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YDJC restrains Th1 cell differentiation by blocking SREBP2-mediated cholesterol biosynthesis to alleviate mucosal inflammation in inflammatory bowel disease

Cellular & Molecular Immunology volume 23, pages 15–30 (2026)Cite this article

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Abstract

YdjC chitooligosaccharide deacetylase homolog (YDJC) has been identified as a susceptibility gene for inflammatory bowel disease (IBD), yet its role in the pathogenesis of IBD, particularly in regulating immune responses in the gut mucosa, remains elusive. In this study, we demonstrated that YDJC expression is downregulated in inflamed mucosa, particularly in the CD4+ T cells of IBD patients, and that Ydjc deficiency promotes CD4+ T-cell proliferation and Th1 cell differentiation, thereby exacerbating acute and chronic colitis in mice. Integrative transcriptomic, proteomic, and metabolomic analyses revealed that Ydjc-/-CD4+ T cells exhibit upregulated SREBP2-mediated cholesterol biosynthesis. Consistently, treatment with key enzyme inhibitors targeting cholesterol biosynthesis, including simvastatin, fatostatin, and AAV-sh-Srebf2, markedly suppressed CD4+ T-cell proliferation and Th1 cell differentiation, thereby alleviating colitis in Ydjc-/- mice. Mechanistically, YDJC directly deacetylates SREBP2, which further suppresses downstream target gene expression (e.g., Hmgcr, Hmgcs1, and Cyp51). Therefore, our findings elucidate a novel mechanism whereby YDJC restrains intestinal mucosal inflammation by downregulating SREBP2-driven Th1 cell differentiation, suggesting that targeting YDJC and SREBP2-mediated cholesterol biosynthesis may serve as promising therapeutic strategies for IBD.

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The data that support the findings of this study are available from the corresponding author upon reasonable request.

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Acknowledgements

We gratefully acknowledge the financial support of the National Natural Science Foundation of China (82370532, 82341219) and Shanghai Hospital Development Center Foundation (SHDC12022118). We thank Professor Youcun Qian (Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, Shanghai) for valuable advice on the experimental design. We also acknowledge the physicians and nurses in the Department of Gastroenterology of Shanghai Tenth People’s Hospital for their assistance with sample collection. We would like to thank BioRender (biorender.com) for providing the tools used to create the scientific illustrations in this manuscript.

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  1. These authors contributed equally: Ai Li, Dengfeng Kang, Zhongsheng Feng, Haifeng Lian.

Authors and Affiliations

  1. Center for Inflammatory Bowel Disease Research and Department of Gastroenterology, The Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai, China

    Ai Li, Dengfeng Kang, Zhongsheng Feng, Xiang Gao, Xiaohan Wu, Han Gao, Xiaoyu Li, Fushun Kou, Jian Lin, Jinghan Hua, Long Ju, Zixuan Xu & Zhanju Liu

  2. Department of Gastroenterology, Yantai Affiliated Hospital of Binzhou Medical University, Yantai, Shandong province, China

    Haifeng Lian

  3. Research Center of Allergy & Immunology, Shenzhen University School of Medicine, Shenzhen, China

    Pingchang Yang

  4. Department of Big Data in Health Science, School of Public Health and The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang province, China

    Xue Li

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Contributions

ZL conceived the study. AL, DK, ZF, and HL designed the experimental protocol, conducted the majority of the experiments and statistical analyses, and drafted the manuscript. XG, HG, XW, XL, FK, JL, JH, PY, and XL contributed to data interpretation. JL and ZX provided the clinical specimens. All the authors reviewed and approved the final manuscript.

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Correspondence to Xue Li or Zhanju Liu.

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Li, A., Kang, D., Feng, Z. et al. YDJC restrains Th1 cell differentiation by blocking SREBP2-mediated cholesterol biosynthesis to alleviate mucosal inflammation in inflammatory bowel disease. Cell Mol Immunol 23, 15–30 (2026). https://doi.org/10.1038/s41423-025-01361-z

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