Oncotarget

Research Papers:

MiR-34a promotes DCs development and inhibits their function on T cell activation by targeting WNT1

Anfei Huang _, Yi Yang, Si Chen, Fei Xia, Di Sun, Deyu Fang, Sidong Xiong, Liping Jin and Jinping Zhang

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Oncotarget. 2017; 8:17191-17201. https://doi.org/10.18632/oncotarget.15228

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Abstract

Anfei Huang1,*, Yi Yang1,*, Si Chen1, Fei Xia1, Di Sun1, Deyu Fang2, Sidong Xiong1, Liping Jin3, Jinping Zhang1

1Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu Province 215123, People’s Republic of China

2Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA

3Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 200040, China

*These authors have contributed equally to the work

Correspondence to:

Jinping Zhang, email: j_pzhang@suda.edu.cn

Liping Jin, email: jinlp01@163.com

Keywords: miR-34a, cDCs, development, IL-17a, T cell activation

Received: July 07, 2016     Accepted: January 16, 2017     Published: February 09, 2017

ABSTRACT

MicroRNAs serve important functions in numerous biological processes. Whether microRNAs also act on dendritic cell (DC) differentiation and function remains unclear. In this study, both conventional DCs (cDCs) and plasmacytoid DCs (pDCs) were increased in miR-34a overexpressing bone marrow chimeric and transgenic (TG) mice. Further experiments showed that miR-34a promoted preDC differentiated into cDCs and pDCs without affecting the proliferation and apoptosis of DCs. Luciferase report assay and Western blot experiments demonstrated that WNT1 is the direct target of miR-34a in DCs. Interestingly, miR-34a overexpressing cDCs also produced a large amount of IL-17a and suppressed T cell activation because of the inhibition of TCF1 expression, thus increasing RORγT expression. Taken together, miR-34a promotes preDC to differentiate into cDCs and pDCs, as well as inhibits the function of cDCs on the activation of CD4+ T cells by producing IL-17a.


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