早期生长反应因子1和2（Egr-1和2）对FcεRI介导的肥大细胞活化和免疫效应分子产生具有重要的调控作用；Egr-2能明显影响肥大细胞诱导的CD4+T细胞迁移。因此，探索早期生长反应因子对肥大细胞免疫效应分子的影响，以及Egr家族对CD4+T细胞迁移活化的调控机制，是本课题的研究目的。首先，应用芯片技术筛选受Egr基因调控的免疫效应分子；第二，用EMSA、CHIP等方法研究Egr基因对目的免疫效应分子的调控机制；第三，应用体外T细胞迁移、活化增殖模型，研究早期生长反应因子对CD4+T细胞迁移、活化增殖的调控机制；第四，应用RNAi干扰等方法构建Egr-1，2联合缺失肥大细胞模型，研究二者是否在CD4+T细胞迁移或活化等方面具有协同互补作用；第五，应用芯片技术等方法研究肥大细胞诱导CD4+T细胞迁移活化的完整信号途径。力争发现新的免疫调控分子，以阐释免疫应答机制和干预过敏性疾病的发生。

Early growth response factor 1 and 2 play important roles in FcεRI-mediated mast cell activation and immune productions. Early growth response factor 2 can significantly affect mast cell induced CD4+T cell migration. Therefore, the purpose of this proposal is to investigate the role of early growth response factor in mast cell derived immune effectors, and the role of early growth response factor family in the regulatory mechanisms of CD4+T cell migration and activation. Firstly, use gene chip or protein chip to screen immune effectors that were regulated by early growth response factor genes. Secondly, use the electrophoresis mobility shift assay (EMSA) or chromatin immunoprecipitation assay (CHIP)to confirm the regulatory mechanisms for early growth response factor gene's target immune effectors. Thirdly, use T cell transwell migration assays, cell activation or proliferation model in vitro to study the regulatory mechanisms of mast cell induced CD4+T cell migration and activation regulated by early growth factor genes. Fourthly, use RNA interference technique to construct Egr-1 and Egr-2 joint deficiency mast cell model, and then investigate whether or not Egr-1 and Egr-2 play a synergetic role in mast cell induced CD4+ T cell migration and activation. Finally, use gene chip and protein chip techniques to investigate the complete signaling pathways in mast cell induced CD4+ T cell migration and activation. Strive to find some new regulatory immune effectors in the process of mast cell induced CD4+ T cell migration and activation. This study will contribute to demonstrate the mechanism of immune response, and prevention or interference with the development and prognosis of hypersensitivity diseases.