哮喘是常见慢性气道炎症性疾病，研究显示Foxp3+Tr发育抑制与哮喘发生相关。我们前期研究发现新生期S.p感染抑制Foxp3+Tr发育促进哮喘发生，但Foxp3+Tr发育抑制机制不清。最新研究发现CD103+DC能促进Foxp3+Tr发育，致病菌感染抑制肠道CD103+DC表达引起Foxp3+Tr发育抑制可致慢性炎症性肠病，新生期S.p感染抑制Foxp3+Tr发育是否与S.p感染抑制肺部CD103+DC表达及功能有关尚未见报道。本课题进一步研究新生期S.p感染对肺CD103+DC表达水平、功能的影响及其与Foxp3+Tr表达相关性，研究S.p感染鼠肺CD103+DC对初始CD4+T细胞分化为Foxp3+Tr的影响，探讨回输CD103+DC对新生期S.p感染实验性哮喘及Foxp3+Tr发育的影响，阐明新生期S.p感染抑制Foxp3+Tr发育促进哮喘发生机制，为防治哮喘提供新思路和理论基础。

Asthma is the most common chronic airway disease in children and the pathogenesis remains unclear. Recent studies suggest that deficiency in Foxp3+Tr may play an important role in the pathogenesis of asthma. Our pilot studies suggest streptococcus pneumoniae (S.p) infection in neonatal mice inhibits Foxp3+Tr development and induce experimental asthma. More recent studies demonstrated CD103+DC can promote Foxp3+Tr development. Intestinal bacterial pathogens have been shown to inhibit CD103+DC expression and the development of Foxp3+Tr which leads to chronic intestinal inflammation. It is not known whether S.p infection in neonatal mice induced inhibition of Foxp3+Tr development is associated with a decreased expression and/or function of CD103+DC. Based on our pilot studies, we aim to study further the effects of neonatal S.p infection on the number and function of CD103+DC, to determine the association between CD103+DC and Foxp3+Tr development and their relation with airway inflammation and hyperresponsiveness of experimental asthma. Through the research we can determine the immune mechanisms of neonatal S.p infection inhibiting Foxp3+Tr development, inform strategies of early intervention to Foxp3+Tr cells development and provide new theoretical foundation for primary prevention and clinical treatment of asthma.