MicroRNA-223-3p modulates dendritic cell function and ameliorates experimental autoimmune myocarditis by targeting the NLRP3 inflammasome
MicroRNA-223-3p modulates dendritic cell function and ameliorates experimental autoimmune myocarditis by targeting the NLRP3 inflammasome
复制标题
MicroRNA-223-3p 通过靶向 NLRP3 炎性体调节树突状细胞功能并改善实验性自身免疫性心肌炎
DOI：
10.1016/j.molimm.2019.10.027
复制
发表时间：
2020-01-01
影响因子：
3.6
通讯作者：
Yu, Bo
中科院分区：
文献类型：
--
作者：
Chen, Liangqi;Hou, Xinyu;Yu, Bo
自身免疫性心肌炎是扩张型心肌病和心力衰竭的一个原因。microRNA调节许多免疫过程，但它们在自身免疫性心肌炎异常炎症中的作用仍不清楚。本研究探讨了miR-223- 3 p在实验性自身免疫性心肌炎（EAM）中的作用。我们发现miR-223.3p在EAM小鼠中的表达明显低于正常小鼠。miR-223- 3 p抑制NLRP 3炎性体表达，促进树突状细胞（DC）向致耐受性DC表型极化。miR-223- 3 p通过抑制抗原呈递DC的功能有效地诱导调节性T细胞（Treg）的产生。转移miR-223- 3 p过表达的DC保护小鼠免受EAM的发展。我们的研究结果表明，miR-223- 3 p参与诱导致耐受性DC表型，并调节自身免疫性心肌炎的耐受性。
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.