2. Academic Validation
  3. Dectin-1 stimulates IL-33 expression in dendritic cells via upregulation of IRF4

Dectin-1 stimulates IL-33 expression in dendritic cells via upregulation of IRF4

  • Lab Invest. 2018 Jun;98(6):708-714. doi: 10.1038/s41374-018-0047-2.
Dongjiao Wang 1,  Sujun Gao 2,  Jintong Chen 3,  Yinghua Zhao 3,  Yuxue Jiang 3,  Xiao Chu 3,  Xiaohua Wang 4,  Ning Liu 1,  Tianxue Qin 2,  Qing Yi 3 5,  Ying Yue 6,  Siqing Wang 7
Affiliations

Affiliations

  • 1 Department of Gynecological Oncology, The First Hospital of Jilin University, Changchun, 130061, China.
  • 2 Department of Hematology, The First Hospital of Jilin University, Changchun, 130061, China.
  • 3 Department of Cancer Immunology, The First Hospital of Jilin University, Changchun, 130061, China.
  • 4 Department of Internal Medicine, Linhai First People's Hospital, Linhai, Zhejiang, 317000, China.
  • 5 Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, 44195, USA.
  • 6 Department of Gynecological Oncology, The First Hospital of Jilin University, Changchun, 130061, China. [email protected].
  • 7 Department of Cancer Immunology, The First Hospital of Jilin University, Changchun, 130061, China. [email protected].
PMID: 29540860 DOI: 10.1038/s41374-018-0047-2
Abstract

Interleukin-33 (IL-33) is a potent contributor to Antiviral immune responses and antitumor immunity. We recently discovered that IL-33 is overexpressed in dectin-1-activated dendritic cells (DCs). However, mechanisms of dectin-1-induced IL-33 expression in DCs remain elusive. Curdlan, an agonist of Dectin-1, was used to mature DCs in this study. We found that dectin-1-induced IL-33 expression in DCs relies on Syk and Raf-1 pathways. By using nuclear factor (NF)-κB inhibitors, we also found that dectin-1-induced IL-33 expression relies on NF-κB signaling. Furthermore, through Syk/Raf-1-NF-κB pathway, Dectin-1 signaling stimulates DCs to overexpress interferon regulatory factor 4 (IRF4), which directly upregulates the expression of IL-33 in dectin-1-activated DCs. Thus, our study provides new insights into the mechanisms of dectin-1-induced IL-33 expression in DCs and may provide new targets for improving DC-based Cancer Immunotherapy.

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