在与其受体复合体结合后,CD6触发了actomyosin细胞骨架的重塑
Nozha Borjini1, Yu Lun1, Geen-Fu Jang2
1Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Ave, Cleveland, OH 44195, United States.
Journal of leukocyte biology
|October 11, 2023
概括
研究人员发现CD44是T细胞标记物CD6.6的新受体. CD6与CD44,CD166和CDCP1结合,通过重塑细胞骨架来破坏视网膜色素表皮细胞屏障.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 生物化学 生化学
背景情况:
- T细胞标记物CD6通过与目标细胞上的受体相互作用,在炎症反应中发挥作用.
- 针对CD6的特定受体和目标细胞下游细胞事件尚未完全理解.
研究的目的:
- 确定新的CD6受体并阐明CD6参与影响细胞,特别是视网膜色素表皮 (RPE) 细胞的细胞机制.
主要方法:
- 使用近距离标签来识别潜在的CD6受体.
- 生物化学和生物物理方法证实了CD6及其受体之间的相互作用.
- 在 CD6 刺激后对 RPE 细胞的细胞骨架重塑和紧结完整性的分析.
主要成果:
- CD44被确定为一种新的CD6受体.
- 结合CD6诱导了CD44,CD166和CDCP1在RPE细胞上的聚类.
- CD6刺激通过RhoA/ROCK信号发送触发了actomyosin细胞骨架的重塑,从而导致肌酸酶II酸化的增加.
- 这种细胞骨激活导致紧密连接的分解,损害了RPE屏障的完整性.
结论:
- CD44是CD6的新型受体,与CD166和CDCP1.1形成三方复合体.
- CD6与该复合体的接触激活RhoA/ROCK信号,导致actomyosin重塑和破坏RPE屏障功能.
- 这些发现揭示了在炎症期间T细胞介导的组织屏障破坏机制.
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