相关实验视频
Updated: Sep 20, 2025

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Flow Cytometry-based Assay for the Monitoring of NK Cell Functions
Published on: October 30, 2016
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骨质母细胞通过RANK/RANKL在多发性髓瘤中抑制NK细胞杀死功能
Nanhao Meng1,2,3, Xueke Zhu1,2,3, Nannan Xie1,2,3
1Department of Hematology, Tianjin Medical University General Hospital, Tianjin, China.
概括
多发性骨髓瘤骨质母细胞通过RANK/RANKL通路损害自然杀手 (NK) 细胞的功能. 用denosumab阻断RANKL可增强NK细胞活性,并诱导髓瘤细胞亡,提供一种潜在的治疗策略.
科学领域:
- 血液学 血液学 血液学
- 免疫学 免疫学 免疫学
- 在瘤学瘤学.
背景情况:
- 多发性骨髓瘤 (MM) 是一种无法治愈的血液性恶性瘤.
- 骨髓免疫微环境对于MM的进展至关重要.
- 众所周知,MM患者的自然杀手 (NK) 细胞功能被耗尽.
研究的目的:
- 研究MM中NK细胞枯竭的机制.
- 确定与MM骨质母细胞和NK细胞功能相关的治疗点.
主要方法:
- 在MM患者中分析了NK细胞中NF-kappa B (RANK) 表达的受体激活剂和NF-kappa B连接物 (RANKL) 水平的血清受体激活剂.
- 评估了骨质母细胞与中酶体干细胞在RANKL分泌中的作用.
- 评估了德诺苏马布 (RANKL抑制剂) 对NK细胞标记物 (CD107a,KIR3DL1,穿孔素,大酶B) 和MM细胞亡的影响.
主要成果:
- 与对照人群相比,MM患者的NK细胞和RANKL水平上升的RANK表达.
- MM细胞诱导NK细胞上的RANK表达.
- 骨质母细胞,而不是介酶干细胞,是RANKL的主要来源.
- 德诺苏马布治疗增加了NK细胞激活标记物和细胞毒性潜力,并增强了MM细胞亡.
结论:
- 骨髓骨质母细胞通过RANK/RANKL通路抑制MM中的NK细胞功能.
- 德诺苏马布显示出恢复NK细胞功能和治疗MM的潜力.
- 与登苏马布和免疫调节药物 (列纳利多米德,波马利多米德) 的联合治疗可以改善MM患者的NK细胞功能.
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