Exogenous interleukin 37 ameliorates atherosclerosis via inducing the Treg response in ApoE-deficient mice

Abstract Our previous study indicated that interleukin (IL)-37 is involved in atherosclerosis. In the present study, Anterior tibial arteries were collected from diabetes patients and controls. A histopathological analysis showed that IL-37 was over-expressed in human atherosclerotic plaques. Many t...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Qingwei Ji, Kai Meng, Kunwu Yu, Song Huang, Ying Huang, Xiaohong Min, Yucheng Zhong, Bangwei Wu, Yuzhou Liu, Shaoping Nie, Jianwei Zhang, Yujie Zhou, Qiutang Zeng
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2017
Materias:
R
Q
Acceso en línea:https://doaj.org/article/a43be55c370f4b809398b558ce3cf014
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:a43be55c370f4b809398b558ce3cf014
record_format dspace
spelling oai:doaj.org-article:a43be55c370f4b809398b558ce3cf0142021-12-02T16:06:54ZExogenous interleukin 37 ameliorates atherosclerosis via inducing the Treg response in ApoE-deficient mice10.1038/s41598-017-02987-42045-2322https://doaj.org/article/a43be55c370f4b809398b558ce3cf0142017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-02987-4https://doaj.org/toc/2045-2322Abstract Our previous study indicated that interleukin (IL)-37 is involved in atherosclerosis. In the present study, Anterior tibial arteries were collected from diabetes patients and controls. A histopathological analysis showed that IL-37 was over-expressed in human atherosclerotic plaques. Many types of cells including macrophages, vascular smooth muscle cells (VSMCs), endothelial cells and T lymphocyte expressed IL-37 in human atherosclerotic plaques. ApoE−/− mice were divided into a control group and a recombinant human IL-37-treated group. The IL-37 treatment resulted in a significant decrease in macrophages and CD4+ T lymphocytes and a substantial increase in VSMCs and collagen in atherosclerotic plaques, resulting in a reduction in atherosclerotic plaque size. Furthermore, the IL-37 treatment modulated the CD4+ T lymphocyte activity, including a decrease in T helper cell type 1 (Th1) and Th17 cells and an increase in regulatory T (Treg) cells, and inhibited the maturity of dendritic cells both in vivo and in vitro. In addition, treatment with anti-IL-10 receptor monoclonal antibody abrogated the anti-atherosclerotic effects of IL-37. These data suggest that exogenous IL-37 ameliorates atherosclerosis via inducing the Treg response. IL-37 may be a novel therapeutic to prevent and treat atherosclerotic disease.Qingwei JiKai MengKunwu YuSong HuangYing HuangXiaohong MinYucheng ZhongBangwei WuYuzhou LiuShaoping NieJianwei ZhangYujie ZhouQiutang ZengNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Qingwei Ji
Kai Meng
Kunwu Yu
Song Huang
Ying Huang
Xiaohong Min
Yucheng Zhong
Bangwei Wu
Yuzhou Liu
Shaoping Nie
Jianwei Zhang
Yujie Zhou
Qiutang Zeng
Exogenous interleukin 37 ameliorates atherosclerosis via inducing the Treg response in ApoE-deficient mice
description Abstract Our previous study indicated that interleukin (IL)-37 is involved in atherosclerosis. In the present study, Anterior tibial arteries were collected from diabetes patients and controls. A histopathological analysis showed that IL-37 was over-expressed in human atherosclerotic plaques. Many types of cells including macrophages, vascular smooth muscle cells (VSMCs), endothelial cells and T lymphocyte expressed IL-37 in human atherosclerotic plaques. ApoE−/− mice were divided into a control group and a recombinant human IL-37-treated group. The IL-37 treatment resulted in a significant decrease in macrophages and CD4+ T lymphocytes and a substantial increase in VSMCs and collagen in atherosclerotic plaques, resulting in a reduction in atherosclerotic plaque size. Furthermore, the IL-37 treatment modulated the CD4+ T lymphocyte activity, including a decrease in T helper cell type 1 (Th1) and Th17 cells and an increase in regulatory T (Treg) cells, and inhibited the maturity of dendritic cells both in vivo and in vitro. In addition, treatment with anti-IL-10 receptor monoclonal antibody abrogated the anti-atherosclerotic effects of IL-37. These data suggest that exogenous IL-37 ameliorates atherosclerosis via inducing the Treg response. IL-37 may be a novel therapeutic to prevent and treat atherosclerotic disease.
format article
author Qingwei Ji
Kai Meng
Kunwu Yu
Song Huang
Ying Huang
Xiaohong Min
Yucheng Zhong
Bangwei Wu
Yuzhou Liu
Shaoping Nie
Jianwei Zhang
Yujie Zhou
Qiutang Zeng
author_facet Qingwei Ji
Kai Meng
Kunwu Yu
Song Huang
Ying Huang
Xiaohong Min
Yucheng Zhong
Bangwei Wu
Yuzhou Liu
Shaoping Nie
Jianwei Zhang
Yujie Zhou
Qiutang Zeng
author_sort Qingwei Ji
title Exogenous interleukin 37 ameliorates atherosclerosis via inducing the Treg response in ApoE-deficient mice
title_short Exogenous interleukin 37 ameliorates atherosclerosis via inducing the Treg response in ApoE-deficient mice
title_full Exogenous interleukin 37 ameliorates atherosclerosis via inducing the Treg response in ApoE-deficient mice
title_fullStr Exogenous interleukin 37 ameliorates atherosclerosis via inducing the Treg response in ApoE-deficient mice
title_full_unstemmed Exogenous interleukin 37 ameliorates atherosclerosis via inducing the Treg response in ApoE-deficient mice
title_sort exogenous interleukin 37 ameliorates atherosclerosis via inducing the treg response in apoe-deficient mice
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/a43be55c370f4b809398b558ce3cf014
work_keys_str_mv AT qingweiji exogenousinterleukin37amelioratesatherosclerosisviainducingthetregresponseinapoedeficientmice
AT kaimeng exogenousinterleukin37amelioratesatherosclerosisviainducingthetregresponseinapoedeficientmice
AT kunwuyu exogenousinterleukin37amelioratesatherosclerosisviainducingthetregresponseinapoedeficientmice
AT songhuang exogenousinterleukin37amelioratesatherosclerosisviainducingthetregresponseinapoedeficientmice
AT yinghuang exogenousinterleukin37amelioratesatherosclerosisviainducingthetregresponseinapoedeficientmice
AT xiaohongmin exogenousinterleukin37amelioratesatherosclerosisviainducingthetregresponseinapoedeficientmice
AT yuchengzhong exogenousinterleukin37amelioratesatherosclerosisviainducingthetregresponseinapoedeficientmice
AT bangweiwu exogenousinterleukin37amelioratesatherosclerosisviainducingthetregresponseinapoedeficientmice
AT yuzhouliu exogenousinterleukin37amelioratesatherosclerosisviainducingthetregresponseinapoedeficientmice
AT shaopingnie exogenousinterleukin37amelioratesatherosclerosisviainducingthetregresponseinapoedeficientmice
AT jianweizhang exogenousinterleukin37amelioratesatherosclerosisviainducingthetregresponseinapoedeficientmice
AT yujiezhou exogenousinterleukin37amelioratesatherosclerosisviainducingthetregresponseinapoedeficientmice
AT qiutangzeng exogenousinterleukin37amelioratesatherosclerosisviainducingthetregresponseinapoedeficientmice
_version_ 1718384796887941120