I型干扰素在系统性红斑狼中以Tie2依赖的方式诱导内皮质不稳定
Carlos Rafael-Vidal1,2, Sara Martínez-Ramos1,2, Beatriz Malvar-Fernández1,2
1Rheumatology and Immune-mediated Diseases Group, Galicia Sur Health Research Institute (IIS Galicia Sur), Vigo, Spain.
Frontiers in immunology
|January 1, 2024
概括
I型干扰素 (IFN) 通过抑制Tie2信号来损害系统性红斑狼 (SLE) 的血管稳定性,导致内皮细胞功能障碍和潜在的心血管事件.
科学领域:
- 免疫学 免疫学 免疫学
- 血管生物学 血管生物学
- 类风湿病学 类风湿病学
背景情况:
- 内皮细胞 (EC) 功能障碍和Tie2受体信号传递在系统性红斑狼 (SLE) 病原发生过程中至关重要.
- 炎症过程,特别是I型干扰素 (IFN),与SLE的Tie2通路失调和血管并发症有关.
研究的目的:
- 调查I型IFN在SLE患者中介于Tie2信号诱导的内皮功能障碍中的作用.
- 评估I型IFN和SLE血清对angiopoietin-Tie2轴组件和EC功能的影响.
主要方法:
- 在SLE患者和对照人群中测量了Angiopoietin-1,Angiopoietin-2和溶性Tie1的血清水平.
- 单细胞和人静脉ECs (HUVECs) 被I型IFN或SLE血清刺激.
- 使用qPCR,ELISA,西布洛特,流细胞计,共聚焦显微镜,素和管形成试验,分析了mRNA/蛋白质表达,酸化,转位,EC活力和血管生成.
主要成果:
- 患有SLE的患者表现出升高的sTie1和Ang-2,以及降低的Ang-1,与临床特征相关.
- I型IFN降低了SLE单细胞中的Ang-1,增加了SLE单细胞中的Ang-2,增加了sTie1和Ang-2分泌,同时降低了HUVECs中的Tie2激活.
- I型IFN以Tie2依赖的方式损害了EC活力和血管生成;SLE血清模仿了这些效应,这些效应被Tie1和IFNAR1敲击扭转.
结论:
- I型IFN通过抑制Tie2信号传递,有助于导致SLE内皮细胞不稳定.
- 这些发现表明,一种机制将I型IFN介导的内皮功能障碍与SLE中心血管事件联系在一起.
关键词:
这是一张领带.血管新生素是一种血管新生素.心血管疾病的风险.内皮细胞的破坏稳定系统性红血性狼 (Systemic Lupus Erythematosus) 是一种全身性狼.第一种类型的干扰子干扰子.更多相关视频
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