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Updated: Jan 18, 2026

Assessment of the Immunomodulatory Properties of Human Mesenchymal Stem Cells MSCs

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Published on: December 24, 2015

抑制加勒-3表达可能会在细胞通过过程中保持介质干细胞的免疫调节功能

Minghui Wang¹, Yan Jiang¹, Jiangbo Wan¹

¹Department of Hematology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200090 Shanghai, China.

Frontiers in bioscience (Landmark edition)

|September 8, 2025

概括

介酶干细胞 (MSCs) 由于增加Gal-3.的传递而失去治疗效果. 一种Gal-3抑制剂,TD139,拯救了MSC的免疫调节功能,为移植对宿主疾病治疗提供了一种新的策略.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
再生医学是一种再生医学.

背景情况:

介质细胞干细胞 (MSC) 对于治疗血造细胞干细胞移植后的急性移植对宿主疾病 (aGVHD) 是至关重要的.
广泛的体外扩展是MSC临床使用所必需的,但长期通过会降低它们的治疗疗效.
在传递过程中MSC免疫调节功能障碍背后的机制在很大程度上是未知的.

研究的目的:

研究通过MSCs的免疫调节功能障碍的机制.
探索干预策略,以恢复晚期MSCs的治疗潜力.
评估加勒-3 (Gal-3) 在MSC功能障碍中的作用及其作为治疗点的潜力.

主要方法:

在小鼠aGVHD模型中,早期传递 (P6) 和晚期传递 (P12) MSC之间的治疗效果的比较.
分析不同通道的MSC中的Gal-3表达及其对巨细胞两极分化的影响.
对Gal-3抑制剂TD139评估其恢复MSC免疫调节功能的能力.

主要成果:

晚期通过的MSCs (P12) 与早期通过的MSCs (P6) 相比,在治疗aGVHD方面显著降低了疗效.
在P12MSC中,Gal-3表达显著上调,抑制了抗炎M2型巨细胞两极分化.
TD139治疗剂量依赖性抑制了Gal-3的表达,并恢复了MSCs的免疫调节功能.

结论:

加尔-3的上调有助于MSC免疫调节能力在传递过程中下降.
TD139有效地拯救了晚期MSCs的免疫调节功能障碍.
TD139代表了一种有希望的策略,以提高MSCs在GVHD治疗中的治疗潜力.

关键词:

在GB-0139 (TD139) 中.盖莱克-3的使用方法移植与宿主疾病对比介质细胞干细胞介质细胞干细胞

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