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IL-37 inhibits the maturation of dendritic cells through the IL-1R8-TLR4-NF-kappa B pathway

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机构: [1]Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China [2]Department of Cardiology, the People's Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China [3]Emergency & Critical Care Center, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung, and Blood Vessel Diseases, Beijing 100029, China [4]Department of Cardiology, Handan First Hospital, Handan 056002, China [5]Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China [6]Department of Cardiology, Huadu District People's Hospital of Guangzhou, Guangzhou 510800, China
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关键词: Atherosclerosis IL-37 IL-1R8 TLR4 NF-kappa B Dendritic cell

摘要:
Mature dendritic cells (DCs) play a pathogenic role in atherosclerosis. Our previous study demonstrated that exogenous interleukin (IL)-37 suppresses the maturation of DCs, induces the T-regulatory (Treg) cell response, and attenuates atherosclerosis in ApoE(-/-) mice. The aim of the present study was to explore the molecular mechanism of IL-37 on the maturation of DCs throughout the development of atherosclerosis. The expression of interleukin-1 receptor 8 (IL-1R8), which is a single Ig-domain receptor that was recently found to be pivotal for the extracellular function of IL-37, Toll-like receptor (TLR) 4 and p65, was measured in ApoE(-/-) mice and IL-37 transgenic (IL-37tg) ApoE(-/-) mice. IL-1R8 was mainly expressed in aortic plaque-infiltrated DCs and at significantly higher levels in IL-37tg atherosclerotic mice, accompanied by lower levels of TLR4 and p65. Furthermore, IL-37 eliminated the maturation of DCs induced by oxidized low-density lipoprotein (oxLDL) and caused marked upregulation of IL-1R8 in vitro and downregulation of TLR4 and p65, which was consistent with the experiments in mice. However, the inhibitory effect of IL-37 on the maturation of DCs in vitro was abolished when IL-37 was used to treat DCs isolated from IL-1R8-deficient and TLR4-deficient mice. Therefore, this study indicated that IL-37 inhibited the maturation of DCs via the IL-1R8-TLR4-NF-kappa B pathway and attenuated atherosclerosis in ApoE(-/-) mice.

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出版当年[2018]版:
大类 | 2 区 生物
小类 | 2 区 生化与分子生物学 2 区 生物物理 3 区 细胞生物学
最新[2023]版:
大类 | 2 区 生物学
小类 | 2 区 生物物理 3 区 生化与分子生物学 3 区 细胞生物学
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出版当年[2017]版:
Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Q1 BIOPHYSICS Q2 CELL BIOLOGY
最新[2023]版:
Q1 BIOPHYSICS Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Q2 CELL BIOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2017版] 出版当年五年平均 出版前一年[2016版] 出版后一年[2018版]

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第一作者机构: [1]Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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通讯机构: [1]Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China [2]Department of Cardiology, the People's Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China [3]Emergency & Critical Care Center, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung, and Blood Vessel Diseases, Beijing 100029, China [*1]Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430021, China. [*2]Department of Cardiology, the People's Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China.
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