原生T细胞和人工T细胞的生存优势是通过线粒体从介质干细胞转移而获得的
Angela C Court1,2,3, Eliseo Parra-Crisóstomo2,3, Pablo Castro-Córdova1,3
1IMPACT, Center of Interventional Medicine for Precision and Advanced Cellular Therapy, Santiago, Chile.
Journal of translational medicine
|September 28, 2024
概括
线粒体转移 (MitoT) 保护T细胞免受亡,增强它们的生存能力和免疫治疗的潜力. 这种新的方法提高了CAR-T细胞的活力,为癌症治疗提供了新的途径.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 生物技术是生物技术.
背景情况:
- 亡对于免疫系统的恒温至关重要,但限制了CAR-T细胞治疗的有效性.
- 介酶干细胞/介酶干细胞 (MSCs) 具有免疫调节的特性.
- 之前的研究表明,UC-MSC衍生的线粒体 (MitoT) 将T细胞重新编程成T调节细胞.
研究的目的:
- 评估MitoT对T淋巴细胞和CAR-T细胞亡的影响.
- 研究改善T细胞存活率和免疫治疗代谢适应性的策略.
主要方法:
- 使用无细胞方法 (Mitoception) 进行人工MitoT转移到PBMCs.
- 使用稳素 (STS) 诱导的亡,并使用Annexin V/7AAD和TUNEL试验评估细胞活力.
- 通过流动细胞计,西部斑点和qRT-PCR分析了亡调节剂;评估了电解后的CAR-T细胞亡.
主要成果:
- 转基因受体修饰基因表达与T细胞的亡有关.
- 用MitoT治疗的T细胞表现出对STS诱导的亡的抵抗力.
- MitoT保护了CAR-T细胞免受电穿孔诱导的亡,并显示出细胞毒性活性增加.
结论:
- 人工MitoT通过干扰caspase通路来防止T细胞亡.
- MitoT增强了CAR-T细胞的代谢适应性和抗压能力.
- 基于有机细胞的疗法有可能改善免疫状况和CAR-T治疗结果.
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