前期研究表明，变应性鼻炎是Th2免疫应答占优势，以IgE介导的I型超敏反应为中心环节的局部黏膜炎症。而新近研究证明IL-24在Th2相关的炎性疾病中发挥着非常重要的作用。自发慢性荨麻疹患者针对IL-24的自身抗体IgE的水平和疾病的严重程度呈明显正相关。小鼠实验表明，敲除IL-24的受体亚基IL-20R2可以下调Th2炎症相关细胞因子。我们前期研究发现IL-24在变应性鼻炎患者局部黏膜中的表达也是明显增多的，并且在黏膜上皮也发现了其受体亚基的表达，所以我们推测这些表达增多的IL-24很可能加重了变应性鼻炎的局部炎症。因此，我们拟采用流式细胞技术、体外细胞培养及基因测序等手段对变应性鼻炎中IL-24的来源、上游诱导因素及作用机制进行探索；并通过建立小鼠变应性鼻炎模型，在体验证IL-24在变应性鼻炎中的作用和机制。力图揭示IL-24在变应性鼻炎中扮演的角色，从而为研发新的治疗靶点奠定理论基础。

Previous studies have shown that allergic rhinitis is a local mucosal inflammation dominated by Th2 immune response and centered on type I hypersensitivity mediated by IgE. However, Recent studies have shown that IL-24 plays a very important role in Th2-related inflammatory diseases. The level of IgE against IL-24 in patients with spontaneous chronic urticaria is significantly positively correlated with the severity of the disease. Th2-related inflammatory cytokines were downregulated when receptor subunit IL-20R2 of IL-24 knocked out in mouse. Our recent study found that the expression of IL-24 in the local mucosa of allergic rhinitis patients were also significantly increased, and its recptor subunits were expressed in epithelium. We speculated that the increased expression of IL-24 might aggravate the local inflammation of allergic rhinitis. Therefore, we plan to use flow cytometry, in vitro cell culture and gene sequencing to explore the sources, upstream inducers and mechanisms of IL-24 in allergic rhinitis. The role and mechanism of IL-24 in allergic rhinitis are also verified in vivo by establishing a mouse allergic rhinitis model. This paper aims to reveal the role of IL-24 in allergic rhinitis, thereby laying a theoretical foundation for the development of new therapeutic targets.