MicroRNA-223-3p modulates dendritic cell function and ameliorates experimental autoimmune myocarditis by targeting the NLRP3 inflammasome
| Autor: | Jian Wu, Yong Sun, Min Zhang, Bo Yu, Yang Zheng, Xinyu Hou, Jing Li, Xianghui Zheng, Qingyuan Yang, Maomao Zhang, Nan Gu, Liangqi Chen |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Male Regulatory T cell Inflammasomes Immunology Inflammation Autoimmunity Immune tolerance Autoimmune Diseases 03 medical and health sciences Mice 0302 clinical medicine Immune system microRNA NLR Family Pyrin Domain-Containing 3 Protein Immune Tolerance Medicine Animals Molecular Biology Mice Inbred BALB C business.industry Inflammasome Dendritic cell Dendritic Cells Phenotype Mice Inbred C57BL Disease Models Animal MicroRNAs Myocarditis 030104 developmental biology medicine.anatomical_structure medicine.symptom business 030215 immunology medicine.drug |
| Zdroj: | Molecular immunology. 117 |
| ISSN: | 1872-9142 |
| Popis: | Autoimmune myocarditis is a cause of dilated cardiomyopathy and heart failure. MicroRNAs regulate many immune processes, but their role in aberrant inflammation during autoimmune myocarditis remains unclear. In this study, we investigated the role of miR-223-3p in experimental autoimmune myocarditis (EAM). We found that miR-223-3p expression was significantly lower in EAM mice than that in normal mice. miR-223-3p inhibited NLRP3 inflammasome expression, promoting the polarization of dendritic cells (DCs) towards a tolerogenic DC phenotype. miR-223-3p effectively induced regulatory T cell (Treg) generation by inhibiting the function of antigen-presenting DCs. Transfer of miR-223-3p-overexpressing DCs protected mice against the development of EAM. Our findings suggest that miR-223-3p is involved in the induction of the tolerogenic DC phenotype and regulates tolerance in autoimmune myocarditis. |
| Databáze: | OpenAIRE |
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