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Dectin-1-activated dendritic cells trigger potent antitumour immunity through the induction of Th9 cells

Author

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  • Yinghua Zhao

    (Institute of Translational Medicine, The First Hospital of Jilin University)

  • Xiao Chu

    (Institute of Translational Medicine, The First Hospital of Jilin University)

  • Jintong Chen

    (Institute of Translational Medicine, The First Hospital of Jilin University)

  • Ying Wang

    (Institute of Translational Medicine, The First Hospital of Jilin University)

  • Sujun Gao

    (Cancer Center of the First Hospital of Jilin University)

  • Yuxue Jiang

    (Institute of Translational Medicine, The First Hospital of Jilin University)

  • Xiaoqing Zhu

    (Cancer Center of the First Hospital of Jilin University)

  • Guangyun Tan

    (Institute of Translational Medicine, The First Hospital of Jilin University)

  • Wenjie Zhao

    (The First Hospital and Institute of Immunology, Jilin University)

  • Huanfa Yi

    (The First Hospital and Institute of Immunology, Jilin University)

  • Honglin Xu

    (Laboratory of Virology, National Vaccine and Serum Institute)

  • Xingzhe Ma

    (Lerner Research Institute, Cleveland Clinic)

  • Yong Lu

    (Lerner Research Institute, Cleveland Clinic)

  • Qing Yi

    (Institute of Translational Medicine, The First Hospital of Jilin University
    Lerner Research Institute, Cleveland Clinic)

  • Siqing Wang

    (Institute of Translational Medicine, The First Hospital of Jilin University)

Abstract

Dectin-1 signalling in dendritic cells (DCs) has an important role in triggering protective antifungal Th17 responses. However, whether dectin-1 directs DCs to prime antitumour Th9 cells remains unclear. Here, we show that DCs activated by dectin-1 agonists potently promote naive CD4+ T cells to differentiate into Th9 cells. Abrogation of dectin-1 in DCs completely abolishes their Th9-polarizing capability in response to dectin-1 agonist curdlan. Notably, dectin-1 stimulation of DCs upregulates TNFSF15 and OX40L, which are essential for dectin-1-activated DC-induced Th9 cell priming. Mechanistically, dectin-1 activates Syk, Raf1 and NF-κB signalling pathways, resulting in increased p50 and RelB nuclear translocation and TNFSF15 and OX40L expression. Furthermore, immunization of tumour-bearing mice with dectin-1-activated DCs induces potent antitumour response that depends on Th9 cells and IL-9 induced by dectin-1-activated DCs in vivo. Our results identify dectin-1-activated DCs as a powerful inducer of Th9 cells and antitumour immunity and may have important clinical implications.

Suggested Citation

  • Yinghua Zhao & Xiao Chu & Jintong Chen & Ying Wang & Sujun Gao & Yuxue Jiang & Xiaoqing Zhu & Guangyun Tan & Wenjie Zhao & Huanfa Yi & Honglin Xu & Xingzhe Ma & Yong Lu & Qing Yi & Siqing Wang, 2016. "Dectin-1-activated dendritic cells trigger potent antitumour immunity through the induction of Th9 cells," Nature Communications, Nature, vol. 7(1), pages 1-12, November.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12368
    DOI: 10.1038/ncomms12368
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    Cited by:

    1. Ce Tang & Haiyang Sun & Motohiko Kadoki & Wei Han & Xiaoqi Ye & Yulia Makusheva & Jianping Deng & Bingbing Feng & Ding Qiu & Ying Tan & Xinying Wang & Zehao Guo & Chanyan Huang & Sui Peng & Minhu Chen, 2023. "Blocking Dectin-1 prevents colorectal tumorigenesis by suppressing prostaglandin E2 production in myeloid-derived suppressor cells and enhancing IL-22 binding protein expression," Nature Communications, Nature, vol. 14(1), pages 1-21, December.

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