变应性鼻炎（AR）作为全球性健康问题之一，其发病机制尚未明确。2型固有淋巴细胞（ILC2）在适应性免疫反应启动过程起重要作用。我们发现AR急性期外周血ILC2显著升高，和鼻腔分泌物IL-4、IL-13表达正相关；IL-25和IL-33可显著上调ILC2胞内miR-155和上清中IL-4的表达，miR-155和IL-4的水平呈正相关，可能参与/介导调控ILC2分泌IL-4的功能。据此我们提出假设：AR患者鼻黏膜中ILC2受IL-25和IL-33刺激后，胞内高表达的miR-155可能通过靶向c-maf基因促进ILC2表达IL-4，从而促进下游Th2炎症反应。本项目拟通过质粒转染过表达miR-155、siRNA干扰、c-maf基因敲除等方法验证miR-155靶向c-maf基因调控ILC2功能的作用，揭示AR发病中miR-155调控ILC2功能的作用和机制，为建立可能的干预手段寻找到新的分子靶点。

As a global health issues, the pathogenesis of allergic rhinitis (AR) is still undefined. Group 2 Innate Lymphoid Cells (ILC2) play an important role during the activation of adaptive immune response. We have demonstrated that during an acute period of the patients with AR, the ratio of ILC2 in peripheral blood was elevated significantly, and correlated positively with IL-4、IL-13 expression in the nasal discharge. While, miR-155 expression in ILC2 and IL-4 in supernate was significantly up-regulated by IL-25 and IL-33. The positively correlation between miR-155 and IL-4 indicated that miR-155 might participate in/induce ILC2 secreted IL-4. In this case, we make a hypothesis that in the nasal mucous of patient with AR, as the stimulation of IL-25 and IL-33, the overexpression of miR-155 in ILC2, would accelerate IL-4 expression through a target c-maf gene, which accelerating the downstream Th2 inflammation responses. In the recent research, plasmid transfection to overexpression miR-155, siRNA interference, c-maf knock out were used to demonstrate the mechanism of miR-155 targeted c-maf gene to regulating the function of ILC2 in AR, in order to find a new molecular target for the treatment of AR patients.