[1]黄海艳,李子卓,刘小明,等.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[J].中国皮肤性病学杂志,2019,(06):638-643.[doi:10.13735/j.cjdv.1001-7089.201809081]
 HUANG Haiyan,LI Zizhuo,LIU Xiaoming,et al.B-UVB Irradiation Restrains Dendritic Cells-Mediated Th2 Type Responses in Atopic Dermatitis[J].The Chinese Journal of Dermatovenereology,2019,(06):638-643.[doi:10.13735/j.cjdv.1001-7089.201809081]
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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
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《中国皮肤性病学杂志》[ISSN:1001-7089/CN:61-1197/R]

卷:
期数:
2019年06期
页码:
638-643
栏目:
论著
出版日期:
2019-05-16

文章信息/Info

Title:
B-UVB Irradiation Restrains Dendritic Cells-Mediated Th2 Type Responses in Atopic Dermatitis
文章编号:
1001-7089(2019)06-0638-06
作者:
黄海艳李子卓刘小明邹彦芬于波窦侠
北京大学深圳医院皮肤科,广东 深圳518036
Author(s):
HUANG HaiyanLI ZizhuoLIU XiaomingZOU YanfenYU BoDOU Xia
(Department of Dermatology,Peking University Shenzhen Hospital,Shenzhen 518036,China)
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
Keywords:
Atopic dermatitis Dendritic cells Narrow-band ultraviolet B Thymic stromal lymphopoietin
分类号:
R 758.2
DOI:
10.13735/j.cjdv.1001-7089.201809081
文献标志码:
A
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NB-UVB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。
Abstract:
Objective To investigate the possible dendritic cells(DCs)regulating immunological mechanisms of narrow-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 inflammatory 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 down-regulating TSLP and inhibiting DCs cell activation,which might be one of the possible mechanisms for the treatment of AD.

参考文献/References:


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备注/Memo

备注/Memo:
[基金项目] 国家自然科学基金(81502727,81472878); 深圳市卫生计生系统科研项目(201506035)
[作者单位] 北京大学深圳医院皮肤科,广东 深圳518036
[通讯作者] 窦侠,E-mail:drdouxia@163.com
更新日期/Last Update: 2019-05-16