NB-UVB通过调节树突状细胞功能抑制特应性皮炎Th2炎症反应  

NB-UVB Irradiation Restrains Dendritic Cells-Mediated Th2 Type Responses in Atopic Dermatitis

作　　者：黄海艳[1] 李子卓 刘小明 邹彦芬[1] 于波[1] 窦侠[1] HUANG Haiyan;LI Zizhuo;LIU Xiaoming;ZOU Yanfen;YU Bo;DOU Xia(Department of Dermatology, Peking University Shenzhen Hospital, Shenzhen 518036, China)

机构地区：[1]北京大学深圳医院皮肤科

出　　处：《中国皮肤性病学杂志》2019年第6期638-643,共6页The Chinese Journal of Dermatovenereology

基　　金：国家自然科学基金(81502727,81472878);深圳市卫生计生系统科研项目(201506035)

摘　　要：目的探讨树突状细胞(DCs)参与窄谱中波紫外线(NB-UVB)治疗特应性皮炎(AD)可能的免疫学机制。方法在DC2.4细胞系中以TSLP刺激诱导树突状细胞活化继而用NB-UVB照射,观察Th2细胞因子的表达情况,并采用T/B缺陷的Rag1^-/-小鼠制备MC903诱导的AD小鼠模型进行验证。结果在体外DCs培养中,TSLP可促进DCs细胞活化并上调Th2细胞因子表达,经NB-UVB照射后,DCs活化程度降低,Th2细胞因子IL-4(P<0.01)和IL-13(P=0.03)相对表达量下降。在AD小鼠模型中,NB-UVB照射可减轻MC903诱导的AD样皮炎,并且Th2细胞因子IL-4(P<0.01)及IL-13(P<0.01)mRNA相对表达量均显著下调,差异具有统计学意义。在DCs(P<0.01)及小鼠(P<0.01)中,NB-UVB照射所致的免疫抑制作用均伴随着TSLP受体TSLPR表达水平下调,差异均有统计学意义。结论体外实验和动物研究结果提示NB4JVB通过下调TSLPR、抑制DCs细胞活化从而抑制Th2炎症反应是其治疗AD的可能机制之一。Objective To investigate the possible dendritic cells (DCs) regulating immunological mechanisms of naiTow-band UVB (NB-UVB) in treating atopic dermatitis (AD). Methods The dendritic cells (DC2. 4 cell line) were induced by TSLP then irradiated with NB-UVB. The mRNA relative expression of Th2- associated inflammatoiy factors and flow cytometry detected cluster of differentiation (CD) protein levels was observed. These findings were further validated in MC903- induced Rag1^-/- AD mouse model. Results In DC cell line,TSLP could promote the expression of Th2 cytokines and activate DCs. After NB-UVB irradiation, the relative expression of Th2 cytokines and the activation of DCs decreased. The mRNA relative expression level of TSLPR was down-regulated as well. In AD mouse model,lesion observation and skin histopathology showed that NB-UVB irradiation could alleviate AD-like lesions caused by MC903 application. The relative expression levels of Th2 cytokines and TSLPR were significantly down-regulated. Conclusion It suggests that NB-UVB irradiation restrains Th2 type responses by dowregulating TSLP and inhibiting DCs cell activation , which might be one of the possible mechanisms for the treatment of AD.

关 键 词：特应性皮炎 树突状细胞 窄谱中波紫外线 胸腺基质淋巴细胞生成素 

分 类 号：R758.2[医药卫生—皮肤病学与性病学]