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

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 () and Siqing Wang ()
Additional contact information
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
Siqing Wang: Institute of Translational Medicine, The First Hospital of Jilin University

Nature Communications, 2016, vol. 7, issue 1, 1-12

Abstract: 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.

Date: 2016
References: Add references at CitEc
Citations: View citations in EconPapers (2)

Downloads: (external link)
https://www.nature.com/articles/ncomms12368 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12368

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms12368

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().