近几十年来，过敏性疾病（如哮喘等）发病率不断升高，但原因不明。尘螨是引起过敏性疾病最主要的过敏原。流行病学调查显示：环境污染物（如多环芳烃，PAH）与过敏性疾病的发病有十分紧密的关联；研究发现PAH可通过芳香烃受体（AhR）调控树突状细胞（DCs）的成熟与活化，进而影响免疫功能及过敏反应，但具体机制尚不清楚。本项目假设PAH的暴露可通过AhR作用DCs诱导Th2免疫偏移，从而使机体在尘螨过敏原存在的情况下更易发生过敏反应，故提出过敏性哮喘发病的“PAH诱发及叠加效应假说”。本课题拟通过哮喘小鼠模型，模拟人类长期低剂量暴露于PAH中的情况，首次探讨PAH通过AhR信号通路，影响DCs的分化与功能，从而诱导并增加尘螨引起哮喘等过敏性疾病的发生及作用机制。本课题将为过敏性疾病的研究提供一个全新的思路与方向，并为当前环境污染日益加剧的形势下哮喘的预防和治疗提供新的理论依据与策略。

In the recent two decades, epidemiological studies have shown that environmental pollutants are highly associated with the development of asthma. However, its mechanism remains to be defined. This project aims at investigating the mechanisms through which aryl hydrocarbon receptor (AhR) and environmental pollutants mediate exacerbation of allergic asthma. AhR is capable of sensing and responding to environmental stimuli, especially polycyclic aromatic hydrocarbons (PAHs, such as benzopyrene). Upon interaction with ligands, AhR is able toregulate immune response. We proposed that exposure to indoor PAHs is capable of exacerbating house dust mite-mediated allergic asthma through targeting AhR and dendritic cells (DCs). We will simulate the human exposure to indoor PAHs in a mouse model of house dust mite-induced asthma and delineate its mechanistic role in the regulation of the differentiation and function of DCs. This project will provide a new direction of investigation of the mechanisms by which environmental pollutants induce allergic asthma, and will also provide evidence-based strategy for the prevention of, and more effective therapy for, asthma, at the time when air pollution has become a significant problem and asthma prevalence is increasing.