系统性红斑狼疮（SLE）是一种以Th17/Treg细胞失衡为主要免疫学表现的自身免疫性疾病。研究证实非编码RNA参与其中，SLE患者外周血中linc0597表达增加，而miR-92a表达下调。项目组证实趋化因子Fractalkine（FKN）参与了SLE发病机理；FKN可调控狼疮鼠Th17/Treg细胞；敲除细胞FKN基因后linc0597表达明显下调、MAPK信号通路异常、转录负调节，表明linc0597与FKN存在相互作用。预测分析显示miR-92a与linc0597及FKN均存在结合位点。推测linc0597可能通过竞争性抑制miR-92a介导FKN参与的Th17/Treg细胞调控。本研究以此为切入点，通过体内外实验研究linc0597/miR-92a介导FKN调控Th17/Treg细胞在SLE发病中的作用及其转录和MAPK信号机制，为阐明SLE的发病机制提供理论依据和实验基础。

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the imbalance of Th17/Treg cells. It was proved that noncoding RNAs involved in the pathogenesis of SLE, the expression of linc0597 increased and the expression of miR-92a decreased in the peripheral blood of SLE patients. Our previous study confirmed that chemokine Fractalkine (FKN) was involved in the pathogenesis of SLE; FKN can be involved in the regulation of SLE Th17/Treg cells; After knockout of FKN gene, expression of linc0597 was downregulated, MAPK signaling pathway was abnormal and transcription was negatively regulated, which indicates that linc0597 can interact with FKN. The prediction analysis showed that there are binding sites between miR-92a and linc0597 as well as FKN. Therefore, it is conjectured that linc0597 may mediate the regulation of FKN in Th17/Treg cells through competitive inhibition of miR-92a. In this study, we will highlight the regulatory role of FKN on Th17/Treg cells mediated by linc0597/miR-92a in the pathogenesis of systemic lupus erythematosus and its mechanisms through in vivo and in vitro experiments, and then provide theoretical and experimental basis for elucidating the pathogenesis of SLE.