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NRP1 instructs IL-17-producing ILC3s to drive colitis progression

Cellular & Molecular Immunology volume 22, pages 161–175 (2025)Cite this article

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Abstract

Group 3 innate lymphoid cells (ILC3s) control tissue homeostasis and orchestrate mucosal inflammation; however, the precise mechanisms governing ILC3 activity are fully understood. Here, we identified the transmembrane protein neuropilin-1 (NRP1) as a positive regulator of interleukin (IL)-17-producing ILC3s in the intestine. NRP1 was markedly upregulated in intestinal mucosal biopsies from patients with inflammatory bowel disease (IBD) compared with healthy controls. Genetic deficiency of NRP1 reduces the frequency of ILC3s in the gut and impairs their production of IL-17A in an NF-κB signaling-dependent and cell-intrinsic manner. The diminished IL-17A production in ILC3s altered the composition of the microbiota and improved the outcome of dextran sodium sulfate (DSS)-induced colitis. Furthermore, pharmacological inhibition of NRP1 with EG00229 alleviated the severity of colitis. These observations demonstrated the critical role of NRP1 in the control of intestinal ILC3s, suggesting that NRP1 is a potential therapeutic target for IBD.

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Acknowledgements

This work was supported by the following grants: National Natural Science Foundation of China (No. 81925018, 82130049, 82430055, to J.Z.; 82321001 to Y.Y.; and 82225015 to Q.L.). This work was also supported by the National Key Research and Development Project of China (2021ZD0202400, to Q.L.) and the New Cornerstone Science Foundation through the XPLORER PRIZE (to Q.L.). The authors declare that they have no competing financial interests.

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  1. These authors contributed equally: Ying Wang, Jianye Wang, Gaoyu Liu.

Authors and Affiliations

  1. Department of oncology, The Second Hospital of Tianjin Medical University; Tianjin Key Laboratory of Precision Medicine for Sex Hormones and Diseases; Tianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China

    Ying Wang, Jianye Wang, Gaoyu Liu, Lijuan Zhang, Pan Zhou, Zhi Yao, Haitao Wang & Jie Zhou

  2. Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, International Joint Laboratory of Ocular Diseases (Ministry of Education), State Key Laboratory of Experimental Hematology, Tianjin, China

    Ying Wang, Jianye Wang, Gaoyu Liu, Lijuan Zhang, Pan Zhou, Zhi Yao & Jie Zhou

  3. Key Laboratory for Major Obstetric Diseases of Guangdong Province, Center of Reproductive Medicine, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China

    Ying Wang & Yong Fan

  4. Division of Hematology/Oncology, Department of Pediatrics, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China

    Gaoyu Liu

  5. Department of Bioinformatics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China

    Xianfu Yi

  6. Department of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, Tianjin, China

    Jingyi Wu & Hailong Cao

  7. Department of Pharmacology, Tianjin Key Laboratory of Inflammatory Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China

    Ying Yu

  8. Department of Neurology, Tianjin Neurological Institute, Tianjin Institute of Immunology, Tianjin Medical University General Hospital, Tianjin, China

    Qiang Liu

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Contributions

J.Z. conceived and supervised this study. H.W. cosupervised this study. Y.W. and J.W. performed most of the experiments, analyzed the data, and wrote the manuscript. G.L. participated in most of the experiments. X.Y. performed the bioinformatic analysis. J.W., L. Z. and P. Z. participated in the animal experiments. H.C. collected the samples and clinical information of the IBD patients and paired healthy individuals. Y.F., Y. Y., Q.L., Z.Y. provided suggestions for project design.

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Correspondence to Haitao Wang or Jie Zhou.

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The authors declare that they have no competing financial interests. J.Z. is an editorial board member of Cellular & Molecular Immunology, but she has not been involved in the peer review or the decision-making of the article.

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Wang, Y., Wang, J., Liu, G. et al. NRP1 instructs IL-17-producing ILC3s to drive colitis progression. Cell Mol Immunol 22, 161–175 (2025). https://doi.org/10.1038/s41423-024-01246-7

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