近年我国来特应性皮炎（AD）患病率快速上升，生命早期患AD可进一步启动特应性进程，是哮喘等过敏性疾病的主要危险因素，阐明其发病机制并寻找有效的治疗方法具有重大的公共卫生意义。丝聚合蛋白是维持皮肤屏障的中心枢纽，其表达及发挥生理作用除受遗传免疫因素影响外，皮肤内众多蛋白酶类及这些酶类的抑制性蛋白酶LEKTI是其表达代谢的最重要调控通路。我们的前期研究表明LEKTI对AD皮损丝聚合蛋白代谢平衡具有保护作用，但LEKTI通过何种途径影响皮肤屏障及免疫反应还不可知。本项目拟通过小鼠AD模型及AD患者角质形成细胞培养，检测LEKTI对皮肤屏障、免疫平衡的影响，从分子、细胞及整体水平等不同层次探讨LEKTI在调控皮肤屏障及免疫平衡方面的作用机制，为利用LEKTI作为靶点来进行AD的治疗提供理论依据。

The prevalence rate of atopic dermatitis (AD) is rising rapidly in our country recently years. The cutaneous manifestations of atopy during early life often represent the beginning of atopic march and a major risk factor of asthma. To clarify the pathogenesis and find effective treatment method has significance in public health. Filaggrin, encoded by FLG gene, is the key protein to maintain the normal epidermal barrier.In addition to heredity and immunity , the expression and putative functions of FLG in the skin barrier are complicated and many proteases involved in. These proteases and their protease inhibitor lympho-epithelial Kazal-type-related inhibitor (LETKI, encoded by SPINK5 gene) is the most improtant metabolic pathway of FLG.Our previous research showed that LEKTI has protective effect on filaggrin metabolism in AD, however the mechanism is unknown. To reveal the protective effect and mechanism of LEKTI on skin barrier and immunity balance, we set up a protocol of AD mice model and AD patients keratinocyte culture, investigate the effect on skin barrier and immmunity balabce.