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IL-11 induces differentiation of myeloid-derived suppressor cells through activation of STAT3 signalling pathway
This item is licensed under:Creative Commons Attribution 4.0 International
| Title: | IL-11 induces differentiation of myeloid-derived suppressor cells through activation of STAT3 signalling pathway |
| Authors: | Sumida, Kentaro Browse this author | | Ohno, Yosuke Browse this author | | Ohtake, Junya Browse this author | | Kaneumi, Shun Browse this author | | Kishikawa, Takuto Browse this author | | Takahashi, Norihiko Browse this author | | Taketomi, Akinobu Browse this author →KAKEN DB | | Kitamura, Hidemitsu Browse this author →KAKEN DB |
| Issue Date: | 1-Sep-2015 |
| Publisher: | Nature Publishing Group |
| Journal Title: | Scientific Reports |
| Volume: | 5 |
| Start Page: | 13650 |
| Publisher DOI: | 10.1038/srep13650 |
| Abstract: | Myeloid-derived suppressor cells (MDSCs) are immune negative regulators in the tumour microenvironment. Interleukin (IL)-11, a member of IL-6 family cytokines, functions through the unique receptor IL-11 receptor α coupled with the common signal transducer gp130. IL-11-gp130 signalling causes activation of the JAK/STAT3 pathway. IL-11 is highly upregulated in many types of cancers and one of the most important cytokines during tumourigenesis and metastasis. However, the precise effect of IL-11 on differentiation into MDSCs is still unknown. Here, we found that CD11b+CD14+ monocytic MDSCs were generated from peripheral blood mononuclear cells (PBMCs) of healthy donors in the presence of IL-11. IL-11-conditioned PBMCs induced higher expression of immunosuppressive molecules such as arginase-1. A reduction of T-cell proliferation was observed when MDSCs generated in the presence of IL-11 were co-cultured with CD3/CD28-stimulated, autologous T cells of healthy donors. Culture of normal PBMCs with IL-11 led to STAT3 phosphorylation and differentiation into MDSCs via STAT3 activation. We confirmed expressions of both IL-11 and phosphorylated STAT3 in tumour tissues of colorectal cancer patients. These findings suggest that monocytic MDSCs may be induced by IL-11 in the tumour microenvironment. Thus, IL-11-mediated regulation in functional differentiation of MDSCs may serve as a possible target for cancer immunotherapy. |
| Rights: | http://creativecommons.org/licenses/by/4.0/ |
| Type: | article |
| URI: | http://hdl.handle.net/2115/67658 |
| Appears in Collections: | 遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 北村 秀光
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