Oncotarget

Research Papers: Immunology:

Exosomes released by granulocytic myeloid-derived suppressor cells attenuate DSS-induced colitis in mice

Yungang Wang, Jie Tian, Xinyi Tang, Ke Rui, Xinyu Tian, Jie Ma, Bin Ma, Huaxi Xu, Liwei Lu and Shengjun Wang _

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Oncotarget. 2016; 7:15356-15368. https://doi.org/10.18632/oncotarget.7324

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Abstract

Yungang Wang1,2,*, Jie Tian2,*, Xinyi Tang1,*, Ke Rui2, Xinyu Tian2, Jie Ma2, Bin Ma2, Huaxi Xu2, Liwei Lu3, 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, Jiangsu University, Zhenjiang, China

3Department of Pathology, The University of Hong Kong, Hong Kong, China

*These authors contributed equally to this work

Correspondence to:

Shengjun Wang, e-mail: sjwjs@ujs.edu.cn

Keywords: inflammatory bowel disease, exosomes, myeloid-derived suppressor cells, inflammation, Immunology and Microbiology Section, Immune response, Immunity

Received: November 09, 2015     Accepted: January 29, 2016     Published: February 11, 2016

ABSTRACT

Myeloid-derived suppressor cells (MDSC) have been described in inflammatory bowel disease (IBD), but their role in the disease remains controversial. We sought to define the effect of granulocytic MDSC-derived exosomes (G-MDSC exo) in dextran sulphate sodium (DSS)-induced murine colitis. G-MDSC exo-treated mice showed greater resistance to colitis, as reflected by lower disease activity index, decreased inflammatory cell infiltration damage. There was a decrease in the proportion of Th1 cells and an increase in the proportion of regulatory T cells (Tregs) in mesenteric lymph nodes (MLNs) from G-MDSC exo-treated colitis mice. Moreover, lower serum levels of interferon (IFN)-γ and tumor necrosis factor (TNF)-α were detected in G-MDSC exo-treated colitis mice. Interestingly, inhibition of arginase (Arg)-1 activity in G-MDSC exo partially abrogated the spontaneous improvement of colitis. In addition, G-MDSC exo could suppress CD4+ T cell proliferation and IFN-γ secretion in vitro and inhibit the delayed-type hypersensitivity (DTH) response, and these abilities were associated with Arg-1 activity. Moreover, G-MDSC exo promoted the expansion of Tregs in vitro. Taken together, these results suggest that G-MDSC exo attenuate DSS-induced colitis through inhibiting Th1 cells proliferation and promoting Tregs expansion.


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