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Th17/Treg balance is regulated by myeloid-derived suppressor cells in experimental autoimmune myocarditis

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单位: [1]Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. [2]Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. [3]Department of Emergency, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. [4]Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. [5]Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
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关键词: autoimmune myocarditis in experiment balance inflammation myeloid‐derived suppressor cells Th17 cells Treg

摘要:
Autoimmune myocarditis is caused by both innate and adaptive immune responses. Many studies have found that myeloid-derived suppressor cells (MDSCs) suppress T-cell responses and reduce immune tolerance, while MDSCs may serve as a key player in inflammatory responses and pathogenesis in variety of autoimmune diseases. However, research into the role of MDSCs in experimental autoimmune myocarditis (EAM) remains lacking.We discovered that the expansion of MDSCs in EAM was closely related to the severity of myocardial inflammation. At an early stage of EAM, both adoptive transfer (AT) and selective depletion of MDSCs could inhibit the expression of IL-17 in CD4+ cells and downregulate the Th17/Treg ratio, alleviating excessive inflammation of EAM myocarditis. In another experiment, in addition, MDSCs transferred after selective depletion could increase IL-17 and Foxp3 expressions in CD4+ cells, as well as the Th17/Treg ratio, contributing to the aggravation of myocardial inflammation. MDSCs promoted the Th17 cell induction under Th17-polarizing conditions in vitro but suppressed Treg expansion.These findings suggest that MDSCs play a plastic role in sustaining mild inflammation in EAM by shifting Th17/Treg balance.© 2023 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd.

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出版当年[2022]版:
大类 | 4 区 医学
小类 | 4 区 免疫学
最新[2025]版:
大类 | 4 区 医学
小类 | 4 区 免疫学
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出版当年[2021]版:
Q4 IMMUNOLOGY
最新[2023]版:
Q3 IMMUNOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2021版] 出版当年五年平均 出版前一年[2020版] 出版后一年[2022版]

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第一作者单位: [1]Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
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通讯机构: [4]Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. [5]Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. [*1]Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China. [*2]Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
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