前期研究表明，STAT5B通过FOXP3作用于Treg细胞影响变应性鼻炎核心免疫反应。但在变应性鼻炎中机体调控STAT5B的机制尚不清楚。结合既往文献及前期研究基础我们发现，变应性鼻炎鼻黏膜上皮中miR146a表达显著降低，利用靶基因预测软件分析发现，miR146a与STAT5B存在潜在特异性结合位点。由此我们推测，miR146a通过STAT5B调控Treg细胞是变应性鼻炎中的重要调节机制。本研究拟从临床组织标本、细胞体外实验、动物模型三个层面通过免疫组化、蛋白印迹等多种试验方法，验证变应性鼻炎中miR146a与STAT5B的关联性，揭示miR146a调节STAT5B进一步影响变应性鼻炎的机制。本项目有望从miRNA的角度探索在基因水平调控变应性鼻炎Treg细胞的重要问题，有助于进一步阐明变应性鼻炎的发病机制，为将来建立可能的干预手段寻找到新的分子靶点。

Previous studies have shown that STAT5B influenced the core immune response in allergic rhinitis by means of acting on the Treg cell through FOXP3. However, the regulatory mechanism of STAT5B involved in allergic rhinitis is still unclear. On the base of previous literature and studies, we found that the expression of miR146a in nasal mucosa of allergic rhinitis significantly decreased. Furthermore, the target gene prediction software tools indicate there are potentially specific binding sites between miR146a and STAT5B. Therefore,we hypothesize that the targeted regulation of miR146a to Treg cell by STAT5B is an important regulatory mechanism in allergic rhinitis. In order to verify the biological relationships between miR146a and STAT5B and reveal the mechanism how miR146a regulates STAT5B in allergic rhinitis, we propose three approaches at different levels, such as the validation in clinical tissue specimens, a variety of tests using in vitro cell lines and in vivo animal model, including immunohistochemistry, Western blot, and so on. This study is expected to explore the important issue of the gene regulation of Treg cells in allergic rhinitis from the perspective of miRNAs (e.g., miR146a). It will provide clinicians and researchers with new insights to further clarify the pathogenesis of allergic rhinitis and find new molecular targets for possible treatment and intervention in the future.