このエントリーをはてなブックマークに追加
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
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
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.
備考
This is an article published by Spandidos Publications
発行日
2016-11-22
出版物タイトル
International Journal of Oncology
50巻
1号
出版者
Spandidos
開始ページ
66
終了ページ
74
ISSN
1019-6439
NCID
AA10992511
資料タイプ
学術雑誌論文
言語
English
OAI-PMH Set
岡山大学
著作権者
https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
論文のバージョン
publisher
PubMed ID
DOI
Web of Sience KeyUT
関連URL
https://doi.org/10.3892/ijo.2016.3776