已知人类和动物哮喘中存在记忆性T细胞（Tm）。中枢性记忆T细胞（Tcm）分布于外周血，肺特异性记忆T细胞（Trm）位于气道。我们前期研究表明，哮喘病人外周血CD4+T记忆细胞比例远高于正常人，且细胞内"信号转导、转录激活子（STATs）"的亚型间比值失衡，即STAT1/STAT6磷酸化比值较正常人降低。有趣的是,该失衡仅见于记忆性T细胞，而非初始细胞。沉默SOCS3(细胞因子信号抑制子3)可使比值趋于正常。因此，本研究以"SOCS3-STATs轴"为主线，深入探索Tcm（人血标本）和Trm（小鼠哮喘模型）的STAT1/STAT6磷酸化功能状态，及其对Tm分化、增殖和凋亡、细胞因子释放的影响。利用基因沉默法体外改造Tm并回输至受鼠，观察对Tcm，Trm构成池、表型、基因型的影响及其对小鼠气道炎症的改善。力求阐释CD4+T记忆细胞在哮喘慢性炎症维持中的重要作用，为开发哮喘新型控制疗法提供新思路

Memory T cells exist in human asthma and asthma animal models.Tcm(Central memory T cell) circulate in peripheral blood,Trm(Resident memory T cells) locate in lung.Our previous research demonstrated the number of Tcm in asthma was more than that in healthy control.STATs (Signal transduction and activator transcription )ratio was imbalance in asthma. It was found STAT1/STAT6 phosphorylation was lower in asthma compared with healthy control.It was interesting that STAT1/STAT6 imbalance was limited to memory T cells,not na?ve T cells.SOCS3(Suppressor of cytokine signals 3) konck-down could make the balance normalization.In this project, we focus on "SOCS3-STATs axis",try to explore the STAT1/STAT6 phosphorylation balance in human blood Tcm and mice lung Trm and the relationship with Tm polarization, proliferation,apoptosis,cytokine profiles.Tm with SOCS3 pre-knock-down is going to infuse back to recipient mice and study how it affect on the number of Tcm,Trm,the phenotype,genotype of Tm and airway inflammation.In this stugy we shed light on the important role of CD4+T memory cells in maintainence of chronic inflammation in asthma,thus provide new way to develop durg or therapy for asthma control.