Oncotarget

Research Papers:

TLR-activated plasmacytoid dendritic cells inhibit breast cancer cell growth in vitro and in vivo

Jing Wu _, Shuang Li, Yang Yang, Shan Zhu, Mingyou Zhang, Yuan Qiao, Yong-Jun Liu and Jingtao Chen

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2017; 8:11708-11718. https://doi.org/10.18632/oncotarget.14315

Metrics: PDF 2782 views  |   HTML 3455 views  |   ?  


Abstract

Jing Wu1, Shuang Li1, Yang Yang1, Shan Zhu1, Mingyou Zhang2, Yuan Qiao1, Yong-Jun Liu1,3, Jingtao Chen1

1Institute of Translational Medicine, The First Hospital, Jilin University, Changchun, 130061, China

2Department of Cardiovascular Center, The First Hospital, Jilin University, Changchun, 130031, China

3Sanofi Research and Development, Cambridge, MA, 02139, USA

Correspondence to:

Jingtao Chen, email: [email protected]

Keywords: breast cancer, plasmacytoid dendritic cells, Toll-like receptor, Imiquimod, CpG

Received: May 10, 2016    Accepted: December 05, 2016    Published: December 28, 2016

ABSTRACT

Plasmacytoid dendritic cells (pDCs) are a unique subset of naturally occurring dendritic cells, which triggers the production of large amounts of type I interferons (IFNs) after viral infections through Toll-like receptor (TLR) 7 and TLR9. Recent studies have demonstrated that the activation of pDCs kills melanoma cells. However, the role of activated pDCs in breast cancer remains to be determined. In the present study, we generated mouse models of breast cancer and demonstrated that activated pDCs can directly kill breast tumor cells through TRAIL and Granzyme B. Furthermore, we established that pDCs initiate the sequential activation of NK cells and CD8+ T cells, and ultimately inhibit breast tumor growth. Understanding the role of activated pDCs in breast cancer may help to develop new strategies for manipulating the function of pDCs and induce anti-tumor immunity in breast cancer.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 14315