ID | 55414 |
フルテキストURL | |
著者 |
Lee, Suni
Department of Hygiene, Kawasaki Medical School
Matsuzaki, Hidenori
Department of Hygiene, Kawasaki Medical School
Maeda, Megumi
Department of Biofunctional Chemistry, Division of Bioscience, Okayama University Graduate School of Natural Science and Technology
Kaken ID
researchmap
Yamamoto, Shoko
Department of Hygiene, Kawasaki Medical School
Kumagai-Takei, Naoko
Hatayama, Tamayo
Department of Hygiene, Kawasaki Medical School
Ikeda, Miho
Department of Hygiene, Kawasaki Medical School
Yoshitome, Kei
Department of Hygiene, Kawasaki Medical School
Nishimura, Yasumitsu
Department of Hygiene, Kawasaki Medical School
Otsuki, Takemi
Department of Hygiene, Kawasaki Medical School
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抄録 | Asbestos exposure causes malignant tumors such as lung cancer and malignant mesothelioma. Based on our hypothesis in which continuous exposure to asbestos of immune cells cause reduction of antitumor immunity, the decrease of natural killer cell killing activity with reduction of NKp46 activating receptor expression, inhibition of cytotoxic T cell clonal expansion, reduced CXCR3 chemokine receptor expression and production of interferon-γ production in CD4+ T cells were reported using cell line models, freshly isolated peripheral blood immune cells from health donors as well as asbestos exposed patients such as pleural plaque and mesothelioma. In addition to these findings, regulatory T cells (Treg) showed enhanced function through cell-cell contact and increased secretion of typical soluble factors, interleukin (IL)-10 and transforming growth factor (TGF)-β, in a cell line model using the MT-2 human polyclonal T cells and its sublines exposed continuously to asbestos fibers. Since these sublines showed a remarkable reduction of FoxO1 transcription factor, which regulates various cell cycle regulators in asbestos-exposed sublines, the cell cycle progression in these sublines was examined and compared with that of the original MT-2 cells. Results showed that cyclin D1 expression was markedly enhanced, and various cyclin-dependent kinase-inhibitors were reduced with increased S phases in the sublines. Furthermore, the increase of cyclin D1 expression was regulated by FoxO1. The overall findings indicate that antitumor immunity in asbestos-exposed individuals may be reduced in Treg through changes in the function and volume of Treg.
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備考 | This is an article published by Spandidos Publications
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発行日 | 2016-11-22
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出版物タイトル |
International Journal of Oncology
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巻 | 50巻
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号 | 1号
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出版者 | Spandidos
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開始ページ | 66
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終了ページ | 74
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ISSN | 1019-6439
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NCID | AA10992511
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資料タイプ |
学術雑誌論文
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言語 |
英語
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OAI-PMH Set |
岡山大学
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著作権者 | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
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論文のバージョン | publisher
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PubMed ID | |
DOI | |
Web of Science KeyUT | |
関連URL | https://doi.org/10.3892/ijo.2016.3776
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