变应性鼻炎(Allergic rhinitis，AR)是一种常见的上呼吸道慢性炎症性疾病, 且是导致哮喘发生的高危因素。以Th2优势分化为主的CD4+ Th 细胞网络失衡是AR的免疫学特征，但导致其免疫失衡的源头--树突状细胞(DC)功能异常的机制尚未阐明。新近研究显示IL-37是DC重要的负性调节分子，具有较强抑制炎症反应作用。本研究拟以AR患者及动物模型为研究对象，以IL-37对DC及下游Th细胞的调控为切入点，通过体内、外实验，明确IL-37在AR患者中的表达及其与AR病情变化间的动态关系，并从DC层面、效应免疫细胞层面及信号通路层面解析IL-37在AR中的调控作用及其可能的机制，以期阐明IL-37通路在AR中的意义，为AR发病机制的研究寻找到重要靶点，并将回答IL-37对AR防治策略的建立是否具有临床应用前景这一重要转化医学问题。

Allergic rhinitis (AR) is a common chronic inflammatory disease of the upper respiratory tract, and it is the leading cause of asthma risk factors. The imbalance of CD4+ T helper cells in allergic rhinitis is characterized by Th2-skewed hyperresponsiveness. However, the source of imbalance of CD4+ T helper cells-dendritic cells (DC) dysfunction has not been elucidated. Recent research show that IL-37 is an important negative molecule of DC, and it plays a strong role in inhibiting inflammatory response. This study will aim to investigate the role of IL-37 in allergic rhinitis. Firstly, we will detect the expression of IL-37 in patients with AR at different stages of the disease. Secondly, we will investigate the effects of IL-37 on the function of DC and the differentiation of CD4+ T helper cells, and then explore the possible signal pathway in this process. Finally, we will confirm the role of IL-37 in AR and evaluate its protective effects through animal models. Generally, the aim of this study is to clarify the role of IL-37 in AR and disclose the immune mechanisms involved in AR through investigating the effects of IL-37 on DC and CD4+ T helper cells. This project will provide an important target for the research of pathogenesis of AR and answer an important translational medicine problem-how to establish new strategies for the prevention and treatment of AR through modulating IL-37.