Abstract |
Asbestos exposure causes lung fibrosis and various malignant tumors such as lung cancer and malignant mesothelioma. The effects of asbestos on immune cells have not been thoroughly investigated, although our previous reports showed that asbestos exposure reduced anti- tumor immunity. The effects of continuous exposure of regulatory T cells (Treg) to asbestos were examined using the HTLV-1 immortalized human T cell line MT-2, which possesses a suppressive function and expresses the Treg marker protein, Foxp3. Sublines were generated by the continuous exposure to low doses of asbestos fibers for more than one year. The sublines exposed to asbestos showed enhanced suppressive Treg function via cell-cell contact, and increased production of soluble factors such as IL-10 and transforming growth factor (TGF)-β1. These results also indicated that asbestos exposure induced the reduction of anti- tumor immunity, and efforts to develop substances to reverse this reduction may be helpful in preventing the occurrence of asbestos-induced tumors.
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Authors | Chen Ying, Megumi Maeda, Yasumitsu Nishimura, Naoko Kumagai-Takei, Hiroaki Hayashi, Hidenori Matsuzaki, Suni Lee, Kei Yoshitome, Shoko Yamamoto, Tamayo Hatayama, Takemi Otsuki |
Journal | Toxicology
(Toxicology)
Vol. 338
Pg. 86-94
(Dec 02 2015)
ISSN: 1879-3185 [Electronic] Ireland |
PMID | 26505785
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. |
Chemical References |
- Asbestos, Serpentine
- CTLA-4 Antigen
- CTLA4 protein, human
- FOXP3 protein, human
- Forkhead Transcription Factors
- Glucocorticoid-Induced TNFR-Related Protein
- IL10 protein, human
- TGFB1 protein, human
- TNFRSF18 protein, human
- Transforming Growth Factor beta1
- Interleukin-10
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Topics |
- Asbestos, Serpentine
(toxicity)
- CTLA-4 Antigen
(metabolism)
- Cell Communication
(drug effects)
- Cell Line, Transformed
- Cell Transformation, Viral
- Coculture Techniques
- Forkhead Transcription Factors
(metabolism)
- Glucocorticoid-Induced TNFR-Related Protein
(metabolism)
- Human T-lymphotropic virus 1
(pathogenicity)
- Humans
- Interleukin-10
(genetics, metabolism)
- Lymphocyte Activation
(drug effects)
- Phenotype
- RNA Interference
- T-Lymphocytes, Regulatory
(drug effects, immunology, metabolism, virology)
- Time Factors
- Transfection
- Transforming Growth Factor beta1
(genetics, metabolism)
- Tumor Escape
(drug effects)
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