促进Foxp3+Treg发育在哮喘防治中有重要作用。我们发现婴儿期PCV7呼吸道免疫促进肺部Foxp3+Treg发育抑制哮喘发生，CD103+DC通过IDO诱导Foxp3+Treg发育，TLR2/4/9激活能促进DC产生IDO，PCV7免疫是否通过TLR2/4/9促进CD103+DC-IDO表达诱导Foxp3+Treg发育抑制哮喘发生未见报道。本课题拟研究TLR2/4/9在PCV7呼吸道免疫对哮喘小鼠CD103+DC-IDO表达水平的影响；研究CD103+DC在婴儿期PCV7呼吸道免疫对哮喘气道炎症、气道高反应性及Foxp3+Treg分化发育的影响；探讨PCV7对CD103+DC诱导Foxp3+Treg发育的影响；探讨IDO对PCV7促进CD103+DC诱导Foxp3+Treg分化发育的影响，阐明PCV7呼吸道免疫诱导Foxp3+Treg发育抑制哮喘发生的机制，为哮喘一级预防提供新思路。

Studies suggest inducing Foxp3+Treg development play important role in asthma. Our previous study indicated infant PCV7 respiratory immunization promote Foxp3+Treg development and inhibit experimental asthma. Recent studies demonstrated CD103+DC can induce Foxp3+Treg development through indoleamine 2,3-Dioxygenase(IDO).IDO production elevated when TLR2/4/9 is actived. It is unclear whether infant PCV7 respiratory immunization can promote CD103+DC-IDO and CD103+DC production through TLR2/4/9 to induce Foxp3+Treg development. We aim to study the role of TLR2/TLR4/TLR9 in infant PCV7 respiratory immunization on the the production of CD103+DC-IDO and CD103+DC during experimental asthma , to investigate the effect of CD103+DC on airway inflammation, airway hyperresponsiveness and Foxp3+Treg development in infant PCV7 immunization mice, to determine PCV7 impact on CD103+DC inducing Foxp3+Treg development and their association with CD103+DC-IDO productions. Through the research we can determine the immune mechanisms of infant PCV7 respiratory immunization inducing Foxp3+Treg development and provide new theoretical foundation for primary prevention and clinical treatment of asthma.