通过ERK/JNK通路和M1巨细胞两极分化,OPN促进白性炎症性细胞因子的表达
Siyi Tang1, Hao Hu1, Manhui Li1
1Shenzhen Key Laboratory for Translational Medicine of Dermatology, Biomedical Research Institute, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, China.
Frontiers in immunology
|January 22, 2024
概括
骨质疏松素 (OPN) 在粉红中升高调节,通过促进M1巨细胞极化和细胞因子产生来驱动炎症. 细胞内和分泌的OPN在这种慢性皮肤疾病中起着不同的作用.
科学领域:
- 免疫皮肤学 免疫皮肤学
- 分子生物学分子生物学
- 蛋白质组学是指蛋白质组学.
背景情况:
- 红是一种慢性炎症性皮肤疾病,与免疫系统调节失调有关.
- 骨质蛋白 (OPN) 是来自免疫细胞的糖蛋白,在粉红病原发生过程中起着未明确的作用.
研究的目的:
- 为了研究骨质疏松素 (OPN) 在病中的作用和表达.
- 为了阐明细胞内OPN (iOPN) 和分泌OPN (sOPN) 在罗莎类炎症中的特定功能.
主要方法:
- 对粉红患者的OPN表达和LL37诱导的皮肤炎症模型的分析.
- 转录组测序以识别OPN调节的途径.
- 在体外实验中使用角质细胞研究OPN对细胞因子产生和信号通路 (ERK1/2,JNK) 的影响.
主要成果:
- 在粉红病患者和实验模型中,OPN表达显著增加.
- OPN调节促炎性细胞因子,并促进M1巨细胞的两极分化.
- 通过ERK1/2和JNK通路,iOPN增强了LL37诱导的IL1B在角质细胞中的产生.
- sOPN调解了角质细胞和巨细胞之间的交叉语音.
结论:
- 骨质疏松素 (OPN) 是粉红病内先天免疫反应的关键调节剂.
- 细胞内 (iOPN) 和分泌 (sOPN) 形式的OPN对病的发病有不同的贡献.
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