机构：[1]Department of Cardiology, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, China[2]Department of Ultrasound, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China[3]Department of Cardiology, Handan First Hospital, Handan 056002, China[4]Department of Cardiology, Renmin Hospital of Wuhan University and Cardiovascular Research Institute, Wuhan University and Hubei Key Laboratory of Cardiology, Wuhan 430060, China[5]Emergency & Critical Care Center, Beijing Anzhen Hospital, Capital Medical University, and 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
Interleukin- (IL-) 35, a novel functional cytokine of regulatory T cells (Treg) comprised of the IL-12p35 subunit and the other subunit Epstein-Barr virus-induced gene 3 (EBI3), regulates the activity of CD4+ T cells and macrophages, thereby playing a critical role in inflammatory and autoimmune diseases. Previous studies demonstrated that both recombinant mice and human IL-35 attenuated atherosclerosis in ApoE-/- mice. Additionally, EBI3 deficiency enhanced the activation of macrophages and increased atherosclerotic lesions in LDLR-/- mice. This study generated double-deficient mice for ApoE and IL-12p35 (ApoE-/- IL-12p35-/- mice) and investigated the effect of IL-12p35 deficiency on atherosclerosis. IL-12p35 deficiency alleviated Th1/Th2 imbalance, aggravated Th17/Treg imbalance, and attenuated atherosclerotic plaque formation in ApoE-/- mice. Additionally, exogenous rIL-35 treatment reversed the imbalance of Th17/Treg and attenuated atherosclerosis in ApoE-/- mice. These findings suggest that IL-12p35 deficiency ameliorates atherosclerosis in ApoE-/- mice, partially, via attenuating the Th1/Th2 imbalance, although IL-12p35 deficiency aggravates the Th17/Treg imbalance.
基金：
National Natural Science Foundation of ChinaNational Natural Science Foundation of China [81460081, 81460061, 81770472, 81760051]
第一作者机构：[1]Department of Cardiology, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, China[2]Department of Ultrasound, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China
通讯作者：
通讯机构：[1]Department of Cardiology, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, China[3]Department of Cardiology, Handan First Hospital, Handan 056002, China
推荐引用方式(GB/T 7714)：
Ying Huang ,Haiying Hu ,Ling Liu ,et al.Interleukin-12p35 Deficiency Reverses the Th1/Th2 Imbalance, Aggravates the Th17/Treg Imbalance, and Ameliorates Atherosclerosis in ApoE-/- Mice[J].MEDIATORS OF INFLAMMATION.2019,2019:-.doi:10.1155/2019/3152040.
APA：
Ying Huang,,Haiying Hu,,Ling Liu,,Jing Ye,,Zhen Wang,...&Yingzhong Lin.(2019).Interleukin-12p35 Deficiency Reverses the Th1/Th2 Imbalance, Aggravates the Th17/Treg Imbalance, and Ameliorates Atherosclerosis in ApoE-/- Mice.MEDIATORS OF INFLAMMATION,2019,
MLA：
Ying Huang,,et al."Interleukin-12p35 Deficiency Reverses the Th1/Th2 Imbalance, Aggravates the Th17/Treg Imbalance, and Ameliorates Atherosclerosis in ApoE-/- Mice".MEDIATORS OF INFLAMMATION 2019.(2019):-
