Interleukin-33 contributes to the induction of Th9 cells and antitumor efficacy by Dectin-1-activated Dendritic cells

Jintong Chen, Yinghua Zhao, Yuxue Jiang, Sujun Gao, Yiming Wang, Dongjiao Wang, Alison Wang, Huanfa Yi, Rui Gu, Qing Yi, Siqing Wang

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


We recently discovered that dectin-1-activated dendritic cells (DCs) drive potent T helper (Th) 9 cell responses and antitumor immunity. However, the underlying mechanisms need to be further defined. The cytokine microenvironment is critical for Th cell differentiation. Here, we show that dectin-1 activation enhances interleukin (IL)-33 expression in DCs. We found that blocking IL-33/ST2 inhibits dectin-1-activated DC-induced Th9 cell differentiation. More importantly, the addition of IL-33 further promotes Th9 cell priming and antitumor efficacy induced by dectin-1-activated DCs. Mechanistically, in addition to the promotion of Th9 and Th1 cells, dectin-1-activated DCs combined with IL-33 abolish the activity of IL-33 in the induction of regulatory T cells. Furthermore, the combined treatment of dectin-1-activated DCs and IL-33 increases the frequencies of CD4+ T cells by fostering their proliferation and inhibiting their exhaustive differentiation. Thus, our results demonstrate the important role of IL-33 in dectin-1-activated DC-induced Th9 cell differentiation and antitumor efficacy, and suggest that the combination of dectin-1-activated DCs and IL-33 may present a new effective modality of DC-based vaccines in tumor immunotherapy.

Original languageEnglish (US)
Article number01787
JournalFrontiers in immunology
StatePublished - Jul 1 2018


  • Cancer immunotherapy
  • Dectin-1
  • Dendritic cells
  • Interleukin-33
  • Th9

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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