IL-33 inhibits the differentiation and immunosuppressive activity of granulocytic myeloid-derived suppressor cells in tumor-bearing mice
- Authors
- Lim, Hui Xuan; Choi, Seulah; Cho, Daeho; Kim, Tae Sung
- Issue Date
- 1월-2017
- Publisher
- WILEY
- Citation
- IMMUNOLOGY AND CELL BIOLOGY, v.95, no.1, pp.99 - 107
- Indexed
- SCIE
SCOPUS
- Journal Title
- IMMUNOLOGY AND CELL BIOLOGY
- Volume
- 95
- Number
- 1
- Start Page
- 99
- End Page
- 107
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/85043
- DOI
- 10.1038/icb.2016.72
- ISSN
- 0818-9641
- Abstract
- Myeloid-derived suppressor cells (MDSCs) contribute to tumor-mediated immune escape by suppressing antitumor immune responses. Interleukin-33 (IL-33) is capable of regulating various immune cell populations; however, the effects of IL-33 on the differentiation of MDSCs have not been well characterized. In this study, we evaluated the effects of IL-33 on MDSCs and found that IL-33 significantly reduced the differentiation of lineage-negative bone marrow progenitor cells into granulocytic MDSCs (G-MDSCs). IL-33-treated MDSCs exhibited diminished immunosuppressive capacity; reduced inhibition on T-cell proliferation and interferon-gamma production, and diminished production of reactive oxygen species. However, IL-33 treatment did not affect the frequency of monocytic MDSCs (M-MDSCs) or their production of nitric oxide and expression of arginase-1. Additionally, compared with control MDSCs, IL-33-treated MDSCs had reduced capacity to induce the differentiation or expansion of Treg cells. Moreover, in vivo IL-33 administration significantly decreased MDSCs and G-MDSCs accumulation in the spleen and tumor microenvironment. Also, despite increasing CD4(+) and CD8(+) T-cell infiltration, IL-33 administration markedly decreased Treg-cell population in tumor microenvironment. Taken together, our findings indicate that IL-33 reduces the frequency and immunosuppressive activity of G-MDSCs and ultimately the extent of tumor growth.
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Collections - Graduate School > Department of Life Sciences > 1. Journal Articles
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