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人类NCF1^90H变体促进IL-23/IL-17-依赖曼南诱导的牛皮病和牛皮病关节炎

Yanpeng Li^1,2, Zhilei Li³, Kutty Selva Nandakumar^2,4

¹Division of Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institute, 17177 Stockholm, Sweden.

Antioxidants (Basel, Switzerland)

|July 29, 2023

概括

一种特定的NCF1基因变异 (NCF1^90H) 导致低反应性氧物种 (ROS) 生产,通过激活关键炎症途径,促进小鼠的牛皮和牛皮关节炎.

科学领域:

免疫学免疫学免疫学
遗传学是一个遗传学.
皮肤病学皮肤病学

背景情况:

NCF1基因中的单核酸变体 (NCF1^R90H) 与自身免疫性疾病有关,这是由于减少反应性氧物种 (ROS) 生产.
牛皮 (PsO) 和牛皮性关节炎 (PsA) 是具有复杂遗传和环境触发因素的炎症性疾病.

研究的目的:

调查NCF1^90H变种在牛皮和牛皮关节炎的发病过程中的作用.
在小鼠模型中阐明了NCF1^90H介导的炎症背后的分子机制.

主要方法:

在使用曼南的小鼠中诱导PsO和PsA通过腹膜内注射或皮肤上应用.
使用流细胞计和免疫染对免疫细胞群 (巨细胞,gδT17细胞) 的分析.
对炎症媒介 (IL-17A,IL-23,TNF-α) 和信号通路 (JAK/STAT) 的基因表达 (RT-qPCR) 和蛋白质水平 (西部斑,免疫组织化学) 的评估.

主要成果:

在小鼠模型 (MIP模型) 中,NCF1^90H变异促进了PsO和PsA的发展.
具有NCF1^90H变异的小鼠表现出过度活化的巨细胞,扩张的角质细胞和增加的γδT17细胞.
在牛皮皮肤组织中观察到IL-17A,IL-23,TNF-α和JAK1/STAT3信号通路的升级.

结论:

NCF1^90H变种作为牛皮和牛皮性关节炎的危险因素.
这种变异激活IL-23/IL-17轴和JAK-STAT信号,导致免疫细胞过度活化和疾病发展.

关键词:

在IL-23/IL-17轴上这就是JAK-STAT.在NCF1中,NCF1是指NCF1.这就是ROSOS ROS.巨细胞是什么?巨细胞是什么?牛皮是一种牛皮.

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