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Decrease in Intracellular Perforin Levels and IFN-γ Production in Human CD8(+) T Cell Line following Long-Term Exposure to Asbestos Fibers

Although the tumorigenicity of asbestos, which is thought to cause mesothelioma, has been clarified, its effect on antitumor immunity requires further investigation. We previously reported a decrease in the percentage of perforin(+) cells of stimulated CD8(+) lymphocytes derived from patients with m...

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Detalles Bibliográficos
Autores principales: Kumagai-Takei, Naoko, Nishimura, Yasumitsu, Matsuzaki, Hidenori, Lee, Suni, Yoshitome, Kei, Otsuki, Takemi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6218727/
https://www.ncbi.nlm.nih.gov/pubmed/30426024
http://dx.doi.org/10.1155/2018/4391731
Descripción
Sumario:Although the tumorigenicity of asbestos, which is thought to cause mesothelioma, has been clarified, its effect on antitumor immunity requires further investigation. We previously reported a decrease in the percentage of perforin(+) cells of stimulated CD8(+) lymphocytes derived from patients with malignant mesothelioma. Therefore, we examined the effects of long-term exposure to asbestos on CD8(+) T cell functions by comparing long-term cultures of the human CD8(+) T cell line EBT-8 with and without exposure to chrysotile (CH) asbestos as an in vitro model. Exposure to CH asbestos at 5 μg/ml or 30 μg/ml did not result in a decrease in intracellular granzyme B in EBT-8 cells. In contrast, the percentage of perforin(+) cells decreased at both doses of CH exposure. CH exposure at 30 μg/ml did not suppress degranulation following stimulation with antibodies to CD3. Secreted production of IFN-γ stimulated via CD3 decreased by CH exposure at 30 μg/ml, although the percentage of IFN-γ(+) cells induced by PMA/ionomycin did not decrease. These results indicate that long-term exposure to asbestos can potentially suppress perforin levels and the production of IFN-γ in human CD8(+) T cells.