IgAN是我国最常见的肾小球肾炎，但确切的发病机制仍不清楚。我们的前期工作证实分泌型IgA（SIgA）能诱导系膜细胞（HRMC)释放炎症因子，提示其具有致病性。但其致病机制有待进一步探讨，为此我们提出假说：SIgA可能通过miRNAs的调控作用，介导HRMC炎症因子的释放。为证实这一假设，我们应用miRNA芯片、生物信息学以及双荧光素酶报告基因检测，发现SIgA可能分别通过调控miR-16-2-3p和miR-100-3p促进HRMC分泌IL-6和IL-8。本课题将通过HRMC、重组慢病毒、患者血、尿、肾组织及小鼠IgAN模型，采用亲和层析、激光共聚焦、实时定量PCR、ELISA、Western blot等技术，从分子、细胞、组织及动物水平明确调控SIgA诱导HRMC炎症因子释放的miRNAs及其作用机制。本研究将从miRNA这个新视点揭示IgAN的发病机制，提供IgAN治疗的新靶点。

IgA nephropathy(IgAN) is the most common glomerulonephritis in our country, but the exact pathogenesis of IgAN is still obscure. Our previous work demonstrated that secretory IgA（SIgA) could induce human renal mesangial cell (HRMC) producing inflammatory factors, which suggests that SIgA is pathogenic. However, the mechanism remains to be further explored. We hypothesize that SIgA induced HRMC inflammatory factors production was regulated by the role of miRNAs. Then, to verify this hypothesis, miRNA chip detection, bioinformatics analysis and dual-luciferase reporter assay system were used, and it was found that SIgA could promote HRMC secretion of IL-6 and IL-8 respectively through the regulation of miR-16-2-3p and miR-100-3p. To further study, in this work, from molecules, cells, tissues and animal levels, HRMC、blood、urine、kidneys of patients and mouse IgAN model will be used to investigate the role and mechanism of miRNAs in HRMC secretion of inflammatory factors induced by SIgA. All the work will be done by the technologies of affinity chromatography, laser confocal, real-time quantitative PCR, ELISA and Western blot, etc. It will explore the pathogenesis of IgAN from the new viewpoint of miRNA and provide new target for the treatment of IgAN.