在T细胞治疗中,化学开关和逆转型细胞因子受体:重编程T细胞以克服固体瘤微环境中的免疫抑制
Riley Rane1,2, Fengqiao Li1,2, Alexis Williams1,2
1Department of Physiology and Biomedical Engineering, Mayo Clinic Arizona, Scottsdale, AZ, United States.
Frontiers in immunology
|October 24, 2025
概括
像化学开关受体 (CSR) 和逆转细胞因子受体 (ICR) 这样的工程受体可以通过克服免疫抑制瘤微环境来增强化学抗原受体 (CAR) T细胞治疗固体瘤.
科学领域:
- 免疫学 免疫学 免疫学
- 在瘤学瘤学.
- 生物技术是生物技术.
背景情况:
- 化学抗原受体 (CAR) T细胞疗法在血液癌症中取得了成功,但在固体瘤中面临挑战.
- 免疫抑制性瘤微环境 (TME) 限制了CAR T细胞的透,持久性和功能.
- 需要新的策略来提高CAR T细胞对固体瘤的疗效.
研究的目的:
- 审查非抗原受体 (CNAR) 的设计,功能和潜力,特别是CSR和ICR.
- 探索CSR和ICR如何在CAR T细胞治疗中克服TME介导的抑制.
- 讨论这些工程受体的临床转化方面的考虑.
主要方法:
- 关于工程T细胞受体的科学文献的综述.
- 对调节T细胞信号的CSR和ICR机制的分析.
- 讨论固体瘤的治疗应用和挑战.
主要成果:
- CSRs将抑制信号转化为激活信号.
- ICRs重定向抑制性细胞因子信号以激活T细胞.
- 无论是CSR还是ICR,都显示出对固体瘤的CART疗法的潜在补充.
结论:
- CSR和ICR提供了有希望的策略,以增强固体瘤中CAR T细胞治疗.
- 对安全性,特异性和临床翻译的进一步研究至关重要.
- 工程受体设计是促进癌症免疫治疗的关键.
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