激活的Tim-3/Galectin-9通过负面调节CD4 T细胞参与了多发性骨髓瘤的发展
Rui Zhang1,2, Shuang Chen1,2, Tingting Luo1,2
1Center of Hematology, the First Affiliated Hospital of Xinjiang Medical University, Xinjiang Uygur Autonomous, Xinjing, People's Republic of China.
Hematology (Amsterdam, Netherlands)
|December 18, 2023
概括
在多发性骨髓瘤 (MM) 患者中,Tim-3/Galectin-9通路升高,与预后较差相关. 阻止这种途径恢复了抗瘤免疫力,这表明它是MM的潜在治疗标.
科学领域:
- 免疫学 免疫学 免疫学
- 在瘤学瘤学.
- 细胞生物学 细胞生物学
背景情况:
- 蒂姆-3/加列克-9相互作用会负面调节T细胞介导免疫.
- 在多发性骨髓瘤 (MM) 中,Tim-3/Galectin-9在CD4 T细胞子集中的作用尚不清楚.
研究的目的:
- 为了研究Tim-3/Galectin-9通路调节CD4T细胞子集和MM的临床预后指标之间的关系.
- 探索Tim-3/Galectin-9作为MM的免疫治疗点的潜力.
主要方法:
- 使用流细胞计,PCR和ELISA检测60名MM患者和40名健康对照的Tim-3和galactin-9表达.
- 在Tim-3/Galectin-9水平和临床预后参数之间进行了相关性分析.
- 进行了体外细胞培养实验,以评估阻断Tim-3/Galectin-9通路的影响.
主要成果:
- 在MM患者中,CD4 T细胞上的Tim-3表达,PBMC中的Galectin-9mRNA和血清Galectin-9蛋白水平显著升高,特别是那些预后指标不佳的患者.
- 蒂姆-3在Th1,Th2和Th17细胞上表达高,但在MM患者的Treg细胞上表达低.
- 阻止Tim-3/Galectin-9通路恢复了抗瘤作用和IFN-γ分泌.
结论:
- 在MM中提升的Tim-3/Galectin-9与通过抑制Th1细胞毒性功能的疾病进展有关,并通过Th2和Th17细胞促进免疫逃逸.
- 蒂姆-3/加勒-9通路代表了多发性骨髓瘤的潜在新型免疫治疗点.
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