高表达IgE高亲和力受体(FcεRI)和Toll样受体2(TLR2)的炎症性树突状表皮细胞（IDEC）在特应性皮炎(AD)的持续和加重中起重要作用。我们在上一个国家自然科学基金课题研究中发现，中重度AD患者单核细胞-IDEC上TLR2活化可通过p38 MAPK上调FcεRI表达，而变应原免疫治疗(ASIT)可显著减轻AD临床症状、改变重要免疫学参数和下调IDEC上FcεRI表达及其介导的促炎症因子分泌。ASIT治疗AD的机制尚不清楚，推测可能与FcεRI和TLR2表达、crosstalk及其介导的IDEC功能改变密切相关。本研究将围绕ASIT治疗前后IDEC的功能变化及其与TLR2-FcεRI表达和crosstalk的联系，从细胞功能、受体表达和信号通路等方面入手，阐明ASIT调控IDEC功能并影响随后T细胞反应的分子机制，为理解ASIT治疗AD的机制和发展新的治疗理念提供理论和实验基础。

The inflammatory dendritic epidermal cells (IDEC) bearing the high-affinity receptor for immunoglobulin E (FcεRI) and Toll-like receptor 2 on their cell surface, plays important roles in the development and maintenance of skin inflammation of atopic dermatitis. In previous study suported by national natural science fund, we have found that, activation of TLR2 could up-regulate the expression of FcεRI on monocytes and IDEC from patients with atopic dermatitis through p38 MAPK, and allergen specific immunotherapy (ASIT) could decrease the severity of clinical symtoms, and change related important immunological parameter, and down-regulate the expression of FcεRI and TLR2 and decrease the cytokine secretion from IDEC. However, the underlying mechanism on the effect of ASIT in AD patients has not been completely clarified. It is is presumed that such regulation is closely to function of IDEC mediated by FcεRI and TLR2. In present study, we will focus on the function changes of IDEC and their relationships with the crosstalk between TLR2 and FcεRI. The aim of present study is to clarify the underlying mechanisms that ASIT lessen the allergic reaction through FcεRI and TLR2 in patients with AD, by comparing the differecnes in function of IDEC, expression of FcεRI and TLR2 and the level of proinflammatory cytokines, T cell response and signal transduction pathway, before and after ASIT. Result of this continual study will provide experimental foundation to understand the mechanism of ASIT for AD patients and develop new immunological treament for AD patients.