系统性红斑狼疮（SLE）研究中一个关键问题是为何会出现B细胞自噬的失调。长链非编码RNA（lncRNA）现被发现在自噬过程中发挥关键作用，但其对狼疮B细胞自噬的调控作用还知之甚少。我们的前期研究中利用RNA测序从B细胞自噬失调的SLE患者中筛选出异常升高的HOXA11-AS，且该lncRNA定位于细胞质、并能特异激活B细胞自噬；还鉴定出可与其竞争性结合的miR-130a-3p，后者能明确调节细胞自噬。因此，我们推测HOXA11-AS/miR-130a-3p通路在调控B细胞自噬中起重要作用；并拟通过自噬流监测、过表达或干扰、结合位点突变、荧光素酶报告及体、内外功能获得/缺失实验探讨HOXA11-AS/miR-130a-3p通路在SLE中调控B细胞自噬的作用机制，评估HOXA11-AS对SLE的诊断、判断疾病活动的临床应用价值；为回答上述SLE关键问题、寻找SLE潜在诊疗靶点提供思路借鉴。

Of note, the exploration of the enhanced autophagic activity mechanism of B cells in systemic lupus erythematosus (SLE) is urgently needed. Several long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are related to autophagy pathway in cancer cells. However, whether lncRNAs and microRNAs participate in the regulation of B cell autophagy remains largely unknown. We performed a high-throughput RNA sequencing to detect the lncRNA expression profiles of human lupus B cells. We found that a novel lncRNA, HOXA11-AS was upregulated in patients with SLE. Overexpression of the HOXA11-AS transcript promoted the autophagy of human primary B cells. Furthermore, dual luciferase reporter assays showed that only miR-130a-3p could directly bind the HOXA11-AS sequence. Previous studies have shown that miR-130a targets ATG2B to inhibit autophagy of chronic lymphocytic leukemia cells. Accordingly, we proposed that the HOXA11-AS-miR-130a-3p axis could regulate the autophagy pathway of B cells in SLE. To confirm this hypothesis, we will explore molecular mechanisms of HOXA11-AS-miR-130a-3p axis and its regulation of the autophagic activity in lupus B cells in vivo and in vitro, by combination of various experiments, including RAN RIP, RNA pull down, luciferase report, inhibition and over-expression, animal experiments, and so on. Our aim is to provide a reference for explorating the mechanism of pathogenic autophagy in lupus B cells and finding a potential diagnostic or therapeutic target for SLE.