变应性鼻炎（AR）为I型变态反应性疾病，我们发现Clara细胞10-KDa蛋白（CC10）通过调控Th17细胞等多种机制参与AR治疗作用，但其作用机制有待深入研究。我们前期研究表明Bregs可以通过多种途径抑制AR临床表型，但其上游调控机制尚不明了。本研究旨在（1）建立AR小鼠模型，通过CC10基因敲除小鼠或者体内给予CC10，体内研究CC10对Bregs调控的相关分子或者细胞机制。（2）体外建立Bregs培养体系，抗体中和、SiRNA干扰或者拮抗剂拮抗其对Bregs作用的相关分子，探讨CC10对Bregs作用的关键分子。（3）建立AR小鼠模型，过继输入CC10作用靶点敲除的Bregs，体内进一步探讨其对Bregs作用及作用的关键分子。本研究通过对AR中CC10对Bregs的调控进行研究，这将有利于我们加深对AR中CC10蛋白作用机理的认识，为CC10的临床治疗提供理论基础。

Allergic rhinitis (AR) is a type I allergic disease and we have shown that CC10 regulated Th17 response in AR, but its mechanism remains unclear. Previously we found that Bregs could relieve clinical manifestations in AR mice in many ways, but its upstream regulatory mechanism awaits further investigation.The study aims to (1)establish an AR model and study the regulation of CC10 on Bregs in a mouse AR model with CC10 knockout mice or CC10 treatment respectively. (2)establish Bregs culture system in vitro with CC10 treatment to investigate the effect of CC10 on bregs with neutralizing,SiRNA interfering and blocking techniques. (3）establish the model of AR, adoptive transfer CC10-treated Bregs in vivo to study the effect of CC10 on Bregs. In this study, we will investigate the regulation of CC10 on bregs in AR, which will help us to deepen the understanding of the mechanism of CC10 in AR, and provide a theoretical basis for the clinical treatment of CC10 in AR.