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临床科室急诊危重症中心首都医科大学附属安贞医院[4]Department of Cardiology, Handan First Hospital, Handan 056002, China[5]Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China临床科室心脏内科中心首都医科大学附属安贞医院[6]Department of Cardiology, Huadu District People's Hospital of Guangzhou, Guangzhou 510800, China
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.
基金:
National Natural Science Foundation of ChinaNational Natural Science Foundation of China [81560085, 8156020265, 81370406]
第一作者机构:[1]Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
共同第一作者:
通讯作者:
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.
推荐引用方式(GB/T 7714):
Liu Tianxiao,Liu Jing,Lin Yingzhong,et al.IL-37 inhibits the maturation of dendritic cells through the IL-1R8-TLR4-NF-kappa B pathway[J].BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS.2019,1864(10):1338-1349.doi:10.1016/j.bbalip.2019.05.009.
APA:
Liu, Tianxiao,Liu, Jing,Lin, Yingzhong,Que, Bin,Chang, Chao...&Ji, Qingwei.(2019).IL-37 inhibits the maturation of dendritic cells through the IL-1R8-TLR4-NF-kappa B pathway.BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS,1864,(10)
MLA:
Liu, Tianxiao,et al."IL-37 inhibits the maturation of dendritic cells through the IL-1R8-TLR4-NF-kappa B pathway".BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS 1864..10(2019):1338-1349