Oncotarget

Reviews:

Interplay between myeloid-derived suppressor cells (MDSCs) and Th17 cells: foe or friend?

Liang Wen, Ping Gong, Chao Liang, Dawei Shou, Baoqing Liu, Yiwen Chen, Changqian Bao, Li Chen, Xiaowei Liu, Tingbo Liang and Weihua Gong _

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Oncotarget. 2016; 7:35490-35496. https://doi.org/10.18632/oncotarget.8204

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Abstract

Liang Wen1,*, Ping Gong2,*, Chao Liang1, Dawei Shou1, Baoqing Liu1, Yiwen Chen1, Changqian Bao1, Li Chen1, Xiaowei Liu3, Tingbo Liang1 and Weihua Gong1

1 Department of Surgery, Second Affiliated Hospital of School of Medicine, Zhejiang University, Hangzhou City, People’s Republic of China

2 Department of Oncology, First Affiliated Hospital of Shihezi University School of Medicine, Shihezi City, People’s Republic of China

3 Division of Gastroenterology, Xiangya Second Hospital, Central South University, Hunan, People’s Republic of China

* These authors have contributed equally to this work

Correspondence to:

Weihua Gong, email:

Tingbo Liang, email:

Xiaowei Liu, email:

Keywords: myeloid-derived suppressor cells; Th17 cells; tumor; autoimmunity; cytokine

Received: December 10, 2015 Accepted: March 02, 2016 Published: March 19, 2016

Abstract

Myeloid-derived suppressor cells (MDSCs) and Th17 cells were first discovered in the fields of cancer and autoimmunity, respectively. In recent years, their activities have been explored in other biological and pathological conditions, such as infective diseases and solid organ transplantation. However, the interplay between MDSCs and Th17 cells and the mechanism of their interaction remain obscure. This review summarized and analyzed the relationship between MDSCs and Th17 cells, both of which participate in tumor, autoimmune disease, infection and other conditions. In tumors, the increase in MDSCs at the tumor site is usually accompanied by the accumulation of Th17 cells. However, their relationship is inconsistent in different tumors. In arthritic mice or rheumatoid arthritis (RA) patients, an increase in MDSCs, which could ameliorate disease symptoms, causes decreased IL-17A gene expression and Th17 cells accumulation. Furthermore, we concluded that the interaction between MDSCs and Th17 cells is mainly mediated by cytokines. However, the mechanisms require further investigation. Determining the details of their interplay will provide a better understanding of immune networks and could lead to the development of immunotherapeutic strategies in the future.


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