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.

中文翻译：

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MicroRNA-223-3p通过靶向NLRP3炎性小体来调节树突状细胞功能并改善实验性自身免疫性心肌炎。

自身免疫性心肌炎是导致扩张型心肌病和心力衰竭的原因。MicroRNA调节许多免疫过程，但在自身免疫性心肌炎期间其在异常炎症中的作用仍不清楚。在这项研究中，我们调查了miR-223-3p在实验性自身免疫性心肌炎（EAM）中的作用。我们发现，EAM小鼠中的miR-223-3p表达明显低于正常小鼠。miR-223-3p抑制NLRP3炎性小体表达，促进树突状细胞（DCs）向耐受性DC表型的极化。miR-223-3p通过抑制抗原呈递DC的功能，有效诱导了调节性T细胞（Treg）的产生。过度表达miR-223-3p的DC的转移可保护小鼠免受EAM的侵害。