lncRNA RP11-231E19.1通过竞争性网络（ceRNA）调控斑秃的机制研究

斑秃（AA）发病机制尚不明确，暂无治愈药物。其临床转归不可预测、易复发、治疗周期长的特点严重影响患者身心健康。前期我们对AA患者外周血T细胞进行lncRNA测序，首次发现lncRNA RP11-231E19.1显著下调，生信分析显示lncRNA RP11-231E19.1/miR-320b/CX3CR1存在竞争性调控网络（ceRNA）。CX3CR1作为趋化因子受体与多种炎症信号密切相关，特别是JAK-STAT信号通路，而后者是诱发斑秃的胞内共同信号。基于此，我们提出lncRNA RP11-231E19.1参与的ceRNA通过竞争性结合调节JAK-STAT信号引起炎症反应，导致毛囊内免疫赦免破坏，引发斑秃。本课题拟通过临床研究和体外实验结合，阐明lncRNA RP11-231E19.1对细胞炎症反应的调控机制，并从整体上建立lncRNA RP11-231E19.1对AA调控的信号传导网络。

The pathogenesis of alopecia areata (AA) is still unclear, and there are no cure drugs. The characteristics of AA including unpredictable clinical outcome, prone to relapse, and long-time treatment seriously affect the physical and mental health of patients. We performed lncRNA sequencing on the peripheral blood T cells of AA, and for the first time found that lncRNA RP11-231E19.1 was significantly down-regulated in AA. Bio-information analysis predicted that there was a competitive regulatory network (ceRNA) between lncRNA RP11-231E19.1/miR-320b/CX3CR1. As a chemokine receptor, CX3CR1 is closely related to a variety of inflammatory signals, especially the JAK-STAT pathway, which is the common intracellular signaling pathway in AA. Then, we propose that the ceRNA which lncRNA RP11-231E19.1 involved regulates the inflammatory response caused by JAK-STAT signal through competitive binding mechanism, leading to immune privilege collapse in hair follicles, resulting AA formation. This project intends to combine clinical and in vitro experiments to clarify the regulation of lncRNA RP11-231E19.1 on cell inflammatory response, and establish a signal transduction network for lncRNA RP11-231E19.1 to regulate AA.