Th2/Th17极化是哮喘免疫病理的根基，但调控机制不明，可能与LncRNA有关。TUG1是高通量技术筛选获得差异表达于哮喘患儿单核细胞的LncRNA。预实验发现过表达LncRNA TUG1可以促进单核-巨噬细胞高表达B7-H3而诱导Th2/Th17细胞极化。B7-H3是Th2/Th17极化的关键分子，也是miR-29c-3p的直接靶基因。过表达或沉默miR-29c-3p可以下调或上调单核-巨噬细胞B7-H3表达。生物信息学预测LncRNA TUG1与miR-29c-3p存在结合位点。因此，推测LncRNA TUG1介导miR-29c-3p调控B7-H3表达促进Th2/Th17极化而在哮喘中起作用。鉴此，本项目通过体内外实验，阐明致敏原诱导LncRNA TUG1表达的作用机制以及LncRNA TUG1介导单核-巨噬细胞调控Th2/Th17极化的作用与机制，为哮喘的免疫干预提供新靶标。

The fountain of immunopathogenesis of asthma is based on Th2 and Th17 cell polarization. The mechanism of Th2 and Th17 cell polarization is still unclear and might be associated with LncRNA. LncRNA TUG1 is identified from children with asthma by differential lncRNA expression profile chips. Our previous study revealed that LncRNA TUG1 could enhance B7-H3 expression in mononuclear macrophage and induce Th2/Th17 polarization. B7-H3 plays vital role in Th2 and Th17 cell polarization and B7-H3 is also the direct target gene of miR-29c-3p. Over expression or Silent expression miR-29c-3p could down-regulated or up-regulated B7-H3 in mononuclear macrophage. There are combining sites between LncRNA TUG1 and miR-29c-3p using bioinformatics. Thus, we hypothesized that LncRNA TUG1 could regulate B7-H3 through miR-29c-3p which could induce Th2/Th17 polarization and play vital role in immunopathogenesis of asthma. Therefore, the specific objectives of this research are to clarify the mechanism of LncRNA TUG1 expression induced by allergen and to explore the role and mechanism of LncRNA TUG1 expression in mononuclear macrophage during regulating Th2/Th17 polarization based on experiments in vitro and vivo. In all, this study is to provide new targets for immunologic intervention of asthma.