Mesenchymal stem cells (MSCs) are identified as a promising tool for the treatment of autoimmune diseases, and several microRNAs (miRNAs) are shown to exhibit vital roles in immune diseases. However, their function and mechanism in systemic lupus erythematosus (SLE) is still unclear. The qRT-PCR analysis was employed to investigate level of miR-153-3p. Subsequently, western blot and luciferase reporter assays were carried out to determine miR-153-3p targets. Cell proliferation and migration were determined using EdU proliferation assays and transwell migration assays. Apoptosis levels were evaluated by annexin V staining and flow cytometry. We used human umbilical cord-derived mesenchymal stem cells (UC-MSCs) transplantation to treat MRL/lpr mice. It was observed that miR-153-3p was upregulated in patients with SLE, and was closely related to SLE disease activity. Overexpression of miR-153-3p decreased UC-MSCs proliferation and migration, and weakened UC-MSCs-mediated decrease of follicular T helper (Tfh) cells and increase of regulatory T (Treg) cells through repressing PELI1 in vitro. We also found that PELI1 overexpression abolished the function of miR-153-3p on UC-MSCs. Furthermore, miR-153-3p overexpression weakened the therapeutic effect of UC-MSCs in MRL/lpr mice in vivo. Taken together, all data suggested that miR-153-3p is a mediator of SLE UC-MSCs regulation and may function as a new therapeutic target for the treatment of lupus.

间充质干细胞（MSCs）被认为是治疗自身免疫性疾病的有前途的工具，并且几种microRNA（miRNAs）被证明在免疫疾病中发挥着至关重要的作用。但是，它们在系统性红斑狼疮（SLE）中的功能和机制仍不清楚。使用qRT-PCR分析研究miR-153-3p的水平。随后，进行了蛋白质印迹和荧光素酶报告基因测定，以确定miR-153-3p靶标。使用EdU增殖测定法和transwell迁移测定法测定细胞增殖和迁移。通过膜联蛋白V染色和流式细胞术评估细胞凋亡水平。我们使用人脐带间充质干细胞（UC-MSCs）移植来治疗MRL / lpr小鼠。观察到SLE患者中miR-153-3p上调，并与SLE疾病活动密切相关。miR-153-3p的过表达降低了UC-MSCs的增殖和迁移，并通过抑制PELI1减弱了UC-MSCs介导的滤泡性T辅助（Tfh）细胞减少和调节性T（Treg）细胞增加。体外。我们还发现，PELI1过表达消除了miR-153-3p在UC-MSC上的功能。此外，miR-153-3p的过表达削弱了UC-MSC在MRL / lpr小鼠体内的治疗效果。综上所述，所有数据表明，miR-153-3p是SLE UC-MSCs调节的介体，并可能作为治疗狼疮的新治疗靶标。