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风湿性关节炎带中的另一个口

Stephanie R Zack¹, Osama Alzoubi¹, Neha Satoeya¹

¹Jesse Brown VA Medical Center and The University of Illinois at Chicago, Chicago, Illinois.

Arthritis & rheumatology (Hoboken, N.J.)

|July 4, 2024

概括

诺奇信号通路在早期类风湿性关节炎 (RA) 中是活跃的,但在后期阶段是不活跃的. 瘤亡因子 (TNF) 影响诺奇配体,虽然一些药物减少了诺奇表达,但抑制剂失败了,这表明需要新的策略.

科学领域:

类风湿病学类风湿病学
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

诺奇信号通路在细胞通信和发育中起着至关重要的作用.
失调的Notch信号已经涉及到各种炎症性疾病,包括类风湿性关节炎 (RA).
了解痕通路在RA病变发生过程中的参与,对于开发向疗法至关重要.

研究的目的:

调查关节炎 (RA) 突组织 (ST) 中的Notch信号通路的作用和调节.
为了确定RA中Notch表达的关键诱导和调节器.
为了评估当前RA治疗对Notch路径组件的疗效.

主要方法:

使用免疫组织化学和电力多普勒超声波分析RA突组织 (ST) 和正常组织中诺奇配体和受体表达的分析.
实验室研究涉及巨细胞 (MΦs),纤维细胞样同胞细胞 (FLS) 和用瘤死因子 (TNF) 刺激的内皮细胞.
通过疾病修饰性抗风湿药物 (DMARD) 和其他生物制剂在共同培养和有机体模型中对Notch路径调节的评估.

主要成果:

切口连接体和受体富含RAST,特别是在MΦs,FLS和内皮细胞上,与早期活性RA和新血管化有关.
托尔类受体和TNF诱导RA细胞中的Notch表达;JAG1和DLL4是关键的诱导性联结体.
抗TNF疗法降低了髓状细胞中的Notch配体的调节;特定的DMARDs降低了JAG1和Notch3的表达,但甲索,IL-6R和B细胞阻断剂是无效的.
NF-κB,MAPK和AKT通路参与了Notch信号发送,而JAK/STAT则没有.

结论:

诺奇信号通路与早期活性RA有关,特别是在新血管化过程中,但不在侵蚀阶段.
TNF是RA中诺奇配体的中心调节者,其抑制会影响诺奇表达.
目前针对Notch信号的治疗策略存在局限性,需要探索RA治疗的替代方法.

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