IL-4,IL-13,TNF-α和IFN-γ通过激活HaCaT细胞中的JAK信号通路来降低CLDN8表达的调节
Xiaojie Wang1, Dandan Mao1, Zhanglei Mu1
1Department of Dermatology, Peking University People's Hospital, Beijing, People's Republic of China.
Clinical, cosmetic and investigational dermatology
|April 29, 2025
概括
克劳丁-8 (CLDN8) mRNA在阿托皮性皮肤炎 (AD) 皮肤中减少,治疗后水平有所改善. 像IL-4,IL-13,TNF-α和IFN-γ这样的细胞因子可能会通过JAK信号来降低CLDN8,而CLDN8蛋白在皮肤中没有被检测到.
科学领域:
- 皮肤病学 皮肤病学
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 紧接口 (TJs) 对于保持皮肤屏障完整性至关重要.
- 甲状腺炎的成分克劳丁-8 (CLDN8) 在皮肤炎条件下被观察到水平降低.
研究的目的:
- 为了研究Claudin-8 (CLDN8) 在亚托皮性皮肤炎 (AD) 中的作用.
- 分析在AD皮肤中的CLDN8mRNA和蛋白质表达,并探索AD相关细胞因子对CLDN8表达的影响.
主要方法:
- 对AD数据集的生物信息分析以评估CLDN8mRNA表达.
- 人类和小鼠皮肤中CLDN8蛋白的免疫组织化学 (IHC).
- 定量聚合酶连锁反应 (qPCR) 用于评估与AD相关的细胞因子和JAK抑制剂治疗的HaCaT细胞中的CLDN8mRNA.
主要成果:
- 发现CLDN8mRNA表达在阿托皮性皮肤炎 (AD) 病变和类似AD的小鼠模型中减少.
- 用dupilumab或crisaborole治疗缓解了CLDN8mRNA的下调.
- 干白素 (IL) -4,IL-13,瘤亡因子 (TNF) -α和干扰素 (IFN) -γ通过JAK激活在HaCaT细胞中降低CLDN8mRNA表达的调节.
- 通过IHC,在人类或小鼠皮肤组织中没有检测到CLDN8蛋白.
结论:
- 在阿托皮性皮肤炎 (AD) 皮肤中,CLDN8 mRNA被降低调节,在治疗期间表达水平恢复.
- 与AD相关的细胞因子 (IL-4,IL-13,TNF-α,IFN-γ) 可能通过JAK信号抑制CLDN8mRNA.
- 皮肤组织中的CLDN8蛋白表达需要进一步研究.
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