目的 ·探讨 miR-322-5p靶向 Akt3抑制 Th17分化对干扰素 β（interferon-β，IFN-β）干预实验性自身免疫性脑脊髓炎（experimental autoimmune encephalomyelitis, EAE）的影响。方法 ·建立 EAE小鼠模型，设 IFN-β干预组和 PBS对照组。流式染色比较 2组 Th17的比例变化； RNA芯片检测 2组小鼠 miRNA的差异表达，筛选出 miR-322-5p做进一步研究；软件预测 miR-322-5p的靶基因为 Akt3；IFN-β干预后和过表达 miR-322-5p后检测 Akt3的表达水平；双荧光素酶报告实验验证 miR-322-5p和 Akt3的直接靶向关系；体外实验观察 Akt3对 Th17细胞分化的影响。结果 · IFN-β干预组的 EAE小鼠 Th17比例均显著降低， miR-322-5p的表达显著升高，而 Akt3的表达明显降低；过表达 miR-322-5p能显著抑制 Akt3的表达，双荧光素酶报告实验显示 Akt3是 miR-322-5p的直接靶基因，且 Akt3对 Th17的体外分化有明显促进作用。结论 · IFN-β可通过影响 miR-322-5p靶向 Akt3，进而抑制 Th17分化来缓解 EAE的疾病进程。

Objective · To investigate the effect of miR-322-5p which targets Akt3 on Th17 differentiation in experimental autoimmune encephalomyelitis (EAE) interferedinterferon-β (IFN-β). Methods · The effect of IFN-β on EAE mice which were randomly divided into IFN-β group and PBS group was examine. The percents of Th17 in the two groups were comparedfluorescence activated cell sorting. The miRNAarray was made to find different miRNAs between those two groups. MiR-322-5p was screened for further research. The target gene of miR-322-5p was predicted using softwares and the common predicted target gene Akt3 was got. The of Akt3 was detected after IFN-β intervention and miR-322-5p over. The target relationship between Akt3 and miR-322-5p was verifiedluciferase reporter assay. At last, the effect of Akt3 on Th17 differentiation was explored in vitro. Results · Comparedto PBSgroup, thepercent of Th17 wassignificantlydownregulated, the ofmiR-322-5p wassignificantlyupregulated and Akt3 was significantly downregulated in IFN-β group. The of Akt3 was obviously decreased after overexpressing miR-322-5p. Luciferase reporter assay showed that Akt3 was directly targetedmiR-322-5p. The percent of Th17 differentiation was greatly promotedAkt3 in vitro. Conclusion · IFN-βsignificantly ameliorates the severityof EAEbyaffecting miR-322-5p whichcan inhibitTh17 differentiationtargeting Akt3.