Th17/Treg balance is regulated by myeloid‐derived suppressor cells in experimental autoimmune myocarditis
Abstract Objective 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 pathogene...
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| Format: | Article |
| Language: | English |
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Wiley
2023-06-01
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| Series: | Immunity, Inflammation and Disease |
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| Online Access: | https://doi.org/10.1002/iid3.872 |
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| author | Xin Xiong Mengjia Yu Dinghang Wang Yange Wang Longxian Cheng |
| author_facet | Xin Xiong Mengjia Yu Dinghang Wang Yange Wang Longxian Cheng |
| author_sort | Xin Xiong |
| collection | DOAJ |
| description | Abstract Objective 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. Methods and Results 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. Conclusion These findings suggest that MDSCs play a plastic role in sustaining mild inflammation in EAM by shifting Th17/Treg balance. |
| format | Article |
| id | doaj-art-cb9a2670c6e84b9d909173589df47521 |
| institution | OA Journals |
| issn | 2050-4527 |
| language | English |
| publishDate | 2023-06-01 |
| publisher | Wiley |
| record_format | Article |
| series | Immunity, Inflammation and Disease |
| spelling | doaj-art-cb9a2670c6e84b9d909173589df475212025-08-20T01:53:08ZengWileyImmunity, Inflammation and Disease2050-45272023-06-01116n/an/a10.1002/iid3.872Th17/Treg balance is regulated by myeloid‐derived suppressor cells in experimental autoimmune myocarditisXin Xiong0Mengjia Yu1Dinghang Wang2Yange Wang3Longxian Cheng4Department of Pediatrics, Tongji Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan ChinaDepartment of Cardiovascular Surgery, Union Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan ChinaDepartment of Emergency, Union Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan ChinaDepartment of Cardiology the First Affiliated Hospital of Zhengzhou University Zhengzhou ChinaLaboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan ChinaAbstract Objective 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. Methods and Results 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. Conclusion These findings suggest that MDSCs play a plastic role in sustaining mild inflammation in EAM by shifting Th17/Treg balance.https://doi.org/10.1002/iid3.872autoimmune myocarditis in experimentbalanceinflammationmyeloid‐derived suppressor cellsTh17 cellsTreg |
| spellingShingle | Xin Xiong Mengjia Yu Dinghang Wang Yange Wang Longxian Cheng Th17/Treg balance is regulated by myeloid‐derived suppressor cells in experimental autoimmune myocarditis Immunity, Inflammation and Disease autoimmune myocarditis in experiment balance inflammation myeloid‐derived suppressor cells Th17 cells Treg |
| title | Th17/Treg balance is regulated by myeloid‐derived suppressor cells in experimental autoimmune myocarditis |
| title_full | Th17/Treg balance is regulated by myeloid‐derived suppressor cells in experimental autoimmune myocarditis |
| title_fullStr | Th17/Treg balance is regulated by myeloid‐derived suppressor cells in experimental autoimmune myocarditis |
| title_full_unstemmed | Th17/Treg balance is regulated by myeloid‐derived suppressor cells in experimental autoimmune myocarditis |
| title_short | Th17/Treg balance is regulated by myeloid‐derived suppressor cells in experimental autoimmune myocarditis |
| title_sort | th17 treg balance is regulated by myeloid derived suppressor cells in experimental autoimmune myocarditis |
| topic | autoimmune myocarditis in experiment balance inflammation myeloid‐derived suppressor cells Th17 cells Treg |
| url | https://doi.org/10.1002/iid3.872 |
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