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Cited 13 time in webofscience Cited 10 time in scopus
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Effects of exposure to extremely low-frequency electromagnetic fields on the differentiation of Th17 T cells and regulatory T cells

Authors
Lee, Yun-JungHyung, Kyeong EunYoo, Jong-SunJang, Ye WonKim, Soo JeongLee, Do IkLee, Sang JoonPark, So-youngJeong, Ji HoonHwang, Kwang Woo
Issue Date
Oct-2016
Publisher
GENERAL PHYSIOL AND BIOPHYSICS
Keywords
EMF; SMAD3; TGF-beta; Th17; Treg
Citation
GENERAL PHYSIOLOGY AND BIOPHYSICS, v.35, no.4, pp 487 - 495
Pages
9
Journal Title
GENERAL PHYSIOLOGY AND BIOPHYSICS
Volume
35
Number
4
Start Page
487
End Page
495
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/1733
DOI
10.4149/gpb_2016011
ISSN
0231-5882
1338-4325
Abstract
The potential risks that electromagnetic fields (EMF) pose to human physiology have been debated for several decades, especially considering that EMF is almost omnipresent and some occupations involve regular exposure to particularly strong fields. In the present study, the effects of 60 Hz 0.3 mT EMF on CD4(+) T cells were evaluated. Production of T cell related cytokines, IFN-gamma and IL-2, was not altered in CD4(+) T cells that were exposed to EMF, and cell proliferation was also unaffected. The expression of genes present in a subset of Th17 cells was upregulated following EMF exposure, and the production of effector cytokines of the IL-17A subset also increased. To determine signaling pathways that underlie these effects, phosphorylation of STAT3 and SMAD3, downstream molecules of cytokines critical for Th17 induction, was analyzed. Increased SMAD3 phosphorylation level in cells exposed to EMF, suggesting that SMAD3 may be at least in part causing the increased Th17 cell production. Differentiation of Treg, another CD4(+) T cell subset induced by SMAD3 signaling, was also elevated following EMF exposure. These results suggest that 60 Hz 0.3 mT EMF exposure amplifies TGF-beta signaling and increases the generation of specific T cell subsets.
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