Blood:巡逻单核细胞可清除血管内皮上黏附的镰状RBC

2019-05-15 MedSci MedSci原创

疼痛性血管闭塞危象(VOC)是镰状细胞病(SCD)最常见的并发症。越来越多的证据表明血管阻塞是由镰状红细胞(RBC)与血管内皮的粘附性增加引起的。因此,从微血管系统中清除内皮细胞上黏附的镰状红细胞有望成为SCD患者改善血流和预防VOC的关键。

中心点:

无论是在体内还是体外,PMos均可清除内皮细胞上黏附的镰状红细胞。

通过控制PMo值可调控镰状体小鼠的血管闭塞。

摘要:

疼痛性血管闭塞危象(VOC)是镰状细胞病(SCD)最常见的并发症。越来越多的证据表明血管阻塞是由镰状红细胞(RBC)与血管内皮的粘附性增加引起的。因此,从微血管系统中清除内皮细胞上黏附的镰状红细胞有望成为SCD患者改善血流和预防VOC的关键。

研究人员推测清除细胞碎片保护血管免受损伤的巡逻单核细胞(PMo)也可清除内皮细胞上粘附的镰状红细胞,从而改善SCD患者的VOC。

研究人员在SCD患者的循环PMos中检测到RBC (GPA+)吞噬物质,在急性危象时其发生频率进一步增加。PMo摄取红细胞对内皮细胞黏附的镰状细胞具有特异性,主要是通过ICAM-1、CD11a和CD18的表达,其不会吞噬对照RBCs。

HO-1诱导通过抵消吞噬的红细胞分解产物的细胞毒性作用提高了PMo的生存能力。此外,输血可通过降低镰状红细胞的摄取提高PMo的存活率。

选择性耗竭镰状体小鼠的PMo可加速血管阻滞和组织损伤,而采用胞壁酰二肽(NOD2配体)治疗可增加PMo数量,减轻阻塞和SCD相关的器官损伤。

总而言之,本研究揭示了一种新的由PMo介导的清除内皮细胞黏附的镰状红细胞的机制,可预防VOC的发生;提示PMo或可成为SCD VOC的新的治疗靶点。

原始出处:

Yunfeng Liu, et al.Patrolling monocytes scavenge endothelial adherent sickle RBC: a novel mechanism of inhibition of vaso-occlusion in SCD. Blood 2019 :blood.2019000172; doi: https://doi.org/10.1182/blood.2019000172

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