Oncotarget

Research Papers:

IL-17A weakens the antitumor immuity by inhibiting apoptosis of MDSCs in Lewis lung carcinoma bearing mice

Juan Wang, Yue Zhang, Kai Yin, Peiqi Xu, Jie Tian, Jie Ma, Xinyu Tian, Yungang Wang, Xinyi Tang, Huaxi Xu and Shengjun Wang _

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Oncotarget. 2017; 8:4814-4825. https://doi.org/10.18632/oncotarget.13978

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Abstract

Juan Wang1,2,4,*, Yue Zhang1,*, Kai Yin3,*, Peiqi Xu2, Jie Tian2, Jie Ma2, Xinyu Tian2, Yungang Wang2, Xinyi Tang2, Huaxi Xu2, Shengjun Wang1,2

1Department of Laboratory Medicine, The Affiliated People’s Hospital, Jiangsu University, Zhenjiang, China

2Institute of Laboratory Medicine, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China

3Department of General Surgery, The Affiliated Hospital, Jiangsu University, Zhenjiang, China

4Department of Laboratory Medicine, Changzhou TCM Hospital, Changzhou, China

*These authors contributed equally to this work

Correspondence to:

Shengjun Wang, email: sjwjs@ujs.edu.cn

Jie Tian, email: tjj850913@163.com

Keywords: myeloid-derived suppressor cells, interleukin-17, apoptosis, tumor immunology

Received: October 04, 2016     Accepted: December 07, 2016     Published: December 16, 2016

ABSTRACT

Myeloid-derived suppressor cells (MDSCs) weaken the antitumor immune response through the inhibition of effector T cell activity and the production of immunosuppressive factors in pathological sites. It is well established that interleukin-17A (IL-17A) has a remarkable role on the promotion of inflammation and tumor formation, and IL-17 has been implicated in the enhancement of immunosuppression of MDSCs, which consequently promotes tumor progression. A detailed study of this relationship remains elusive. In our study, we not only confirmed the promotion of IL-17 on Lewis lung carcinoma (LLC) development but also surprisingly showed that IL-17 could extend the fate and enhance the immunosuppressive effect of MDSCs through activating ERK1/2. Additionally, the effect of IL-17 on MDSCs was reversed, even in tumors by blocking ERK1/2. Interdicting the signaling molecule ERK1/2 could increase the apoptosis of MDSCs and weaken the suppressive activity of MDSCs, so that thereafter, the antitumor immunity could be restored partly. Therefore, these findings offer new insights into the importance of IL-17 and the downstream signaling factor ERK1/2 for MDSCs.


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