变应性鼻炎(AR)的发病率逐年攀升且带来严重的家庭社会负担，其发病机制尚未完全明了。我们在国内外首次证实STAT3、IL17A在AR鼻粘膜中呈特异性高表达，进而测序筛查并验证lncRORγt-AS能上调RORγt，其与STAT3共表达且与AR患者症状评分正相关。为深入研究lncRORγt-AS的作用机制，我们拟在体外调节STAT3及lncRORγt-AS表达，研究STAT3、lncRORγt-AS及RORγt之间表达水平及甲基化/泛素化的变化，同时观察其对Th17细胞的影响;建立AR小鼠模型，合成靶向抑制剂antagoLncRORγt-AS，研究lncRORγt-AS在体内水平对Th17细胞及鼻粘膜炎症的影响。本研究着力于揭示lncRORγt-AS调控Th17细胞反应在AR中的机制，力图阐明lncRORγt-AS在STAT3调控下靶向干预RORγt的潜能，为AR的精准治疗提供新的分子靶点。

The morbidity of allergic rhinitis (AR) has been increasing recent years rapidly and has brought serious family and social burden. However, the mechanisms of pathogenesis remain unclear yet. Our previous studies had confirmed for the first time that STAT3 and IL17A are specifically highly expressed in nasal mucosa of AR. And then a RNA-sequencing assay and followed validation assay confirmed that lncRORγt-AS, which is co-expressed with STAT3 and positively correlated with the symptom score of AR patients, could upregulate the expression of RORγt. An in vitro study of regulating the expression of STAT3 and lncRORγt-AS would be performed to further investigate the mechanisms of the expression level of STAT3, lncRORγt-AS and RORγt and the change of methylation/ubiquitination, at the same time to observe the changes of Th17 cell reaction. An AR mouse model will be established, and the targeted inhibitor antagoLncRORγt-AS will be composed to verify the effect of lncRORγt-AS on Th17 cells and inflammation of nasal mucosa in vivo. This study is devoted to reveal the mechanism of lncRORγt-AS in regulating the cell response of Th17 in AR, and aimed to elucidate the function and potential therapeutic value of lncRORγt-AS in targeting RORγt under the regulation of STAT3. It would provide an anticipated precision therapeutic target for AR.