神经-内分泌应答失衡、调节性T细胞（Treg）数量及抑制功能异常是特应性皮炎（AD）发病的关键因素。课题组前期研究证实利多卡因可在体外通过Smad3/TGF-β信号通路促进Treg细胞分化，并在体内上调Treg细胞表达水平改善AD皮损严重程度。那么利多卡因是否可以调节促肾上腺皮质激素释放激素（CRH）作用下Treg细胞上DOCK8的表达水平？其机制为何？本研究旨在①在体外探讨CRH刺激下人体及小鼠Treg细胞及其上DOCK8、CRHR1、CRHR2的表达水平，检测Treg细胞的抑制功能，并明确以上调节作用是否与Smad3/TGF-β和NF-κB信号通路相关；②在体内检测利多卡因治疗前后AD患者及小鼠模型的血液和皮损中CRH、DOCK8、CRHR1、CRHR2、IL-10，TGF-β的表达水平，结合机体皮损改善程度的差异，探讨是否存在对于利多卡因静脉封闭治疗“更加敏感”的适用人群。

Imbalance of neuro-endocrine response as well as abnormal amount and dysfunction of regulatory T cells (Treg) contribute to the pathogenesis of atopic dermatitis (AD). Our group found that lidocaine could specifically promoted Treg differentiation by activation of TGF-β-induced Smad3 phosphorylation in vitro; Lidocaine therapy also enhanced the percentage of Treg cells in vivo, which was consistent with the decline of SCORAD index. But the effect and mechanism of lidocaine on DOCK8 of Treg cells with CRH stimulation remained unknown. Our aims of the research are as follows: 1) We plan to investigate the expression of Treg cells, DOCK8 and CRHR1/2 in human and mice with the stimulation of CRH in vitro. Furthermore, the suppressive function of Treg cells and the specific pathway need to be verified. 2) We aim to investigate the effect of lidocaine on the expression of CRH, DOCK8, CRHR1/2, IL-10, TGF-β both in blood and lesional skins of AD patients and murine models. We will also take the improvement of SCORAD index into account when we analyze the results and investigate if there is a more sensitive population to the lidocaine therapy.