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Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17

Multiple sclerosis (MS) is an autoimmune disease characterized by T cell infiltration and demyelination of the central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE) is a classical preclinical animal model of MS. In this study, we found that rotating magnetic field (RMF) treat...

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Autores principales: Zhan, Tianying, Wang, Xiaomei, Ouyang, Zijun, Yao, Youli, Xu, Jiangyao, Liu, Shikang, Liu, Kan, Deng, Qiyu, Wang, Yushu, Zhao, Yingying
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185125/
https://www.ncbi.nlm.nih.gov/pubmed/32265343
http://dx.doi.org/10.18632/aging.103018
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author Zhan, Tianying
Wang, Xiaomei
Ouyang, Zijun
Yao, Youli
Xu, Jiangyao
Liu, Shikang
Liu, Kan
Deng, Qiyu
Wang, Yushu
Zhao, Yingying
author_facet Zhan, Tianying
Wang, Xiaomei
Ouyang, Zijun
Yao, Youli
Xu, Jiangyao
Liu, Shikang
Liu, Kan
Deng, Qiyu
Wang, Yushu
Zhao, Yingying
author_sort Zhan, Tianying
collection PubMed
description Multiple sclerosis (MS) is an autoimmune disease characterized by T cell infiltration and demyelination of the central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE) is a classical preclinical animal model of MS. In this study, we found that rotating magnetic field (RMF) treatment exerts potential preventive effects on the discovery of EAE, including reducing the severity of the disease and delaying the onset of the disease. The results indicated that RMF (0.2 T, 4 Hz) treatment increases the accumulation of CD4(+) cells in the spleen and lymph nodes by downregulating the expression of CCL-2, CCL-3 and CCL-5, but has no significant effect on myelin oligodendrocyte glycoprotein (MOG) specific T cell responses. Simultaneously, RMF treatment adjusted the imbalance between regulatory T (Treg) cell and T helper 1 (Th1) cells or T helper 17 (Th17) cells by increasing the proportion of Treg cells and inhibiting the ratio of Th1 and Th17 cell subsets. These findings suggest that exposure to RMF may improve EAE disease by promoting CD4+ cell accumulation into peripheral lymphoid tissue, improving the imbalance between Treg and Th1/Th17 cells. Therefore, as a mild physical therapy approach, RMF, is likely to be a potential way to alter the development of EAE.
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spelling pubmed-71851252020-05-01 Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17 Zhan, Tianying Wang, Xiaomei Ouyang, Zijun Yao, Youli Xu, Jiangyao Liu, Shikang Liu, Kan Deng, Qiyu Wang, Yushu Zhao, Yingying Aging (Albany NY) Research Paper Multiple sclerosis (MS) is an autoimmune disease characterized by T cell infiltration and demyelination of the central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE) is a classical preclinical animal model of MS. In this study, we found that rotating magnetic field (RMF) treatment exerts potential preventive effects on the discovery of EAE, including reducing the severity of the disease and delaying the onset of the disease. The results indicated that RMF (0.2 T, 4 Hz) treatment increases the accumulation of CD4(+) cells in the spleen and lymph nodes by downregulating the expression of CCL-2, CCL-3 and CCL-5, but has no significant effect on myelin oligodendrocyte glycoprotein (MOG) specific T cell responses. Simultaneously, RMF treatment adjusted the imbalance between regulatory T (Treg) cell and T helper 1 (Th1) cells or T helper 17 (Th17) cells by increasing the proportion of Treg cells and inhibiting the ratio of Th1 and Th17 cell subsets. These findings suggest that exposure to RMF may improve EAE disease by promoting CD4+ cell accumulation into peripheral lymphoid tissue, improving the imbalance between Treg and Th1/Th17 cells. Therefore, as a mild physical therapy approach, RMF, is likely to be a potential way to alter the development of EAE. Impact Journals 2020-04-07 /pmc/articles/PMC7185125/ /pubmed/32265343 http://dx.doi.org/10.18632/aging.103018 Text en Copyright © 2020 Zhan et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Zhan, Tianying
Wang, Xiaomei
Ouyang, Zijun
Yao, Youli
Xu, Jiangyao
Liu, Shikang
Liu, Kan
Deng, Qiyu
Wang, Yushu
Zhao, Yingying
Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17
title Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17
title_full Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17
title_fullStr Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17
title_full_unstemmed Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17
title_short Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17
title_sort rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting t cell peripheral accumulation and regulating the balance of treg and th1/th17
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185125/
https://www.ncbi.nlm.nih.gov/pubmed/32265343
http://dx.doi.org/10.18632/aging.103018
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