内源性CD28驱动多发性髓瘤中CAR-T细胞的反应
Mackenzie M Lieberman1, Jason H Tong1, Nkechi U Odukwe1
1Department of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263, USA.
bioRxiv : the preprint server for biology
|April 2, 2024
概括
阻止CD28信号传递在仿制抗原受体 (CAR) T细胞中,阻碍了它们对多发性骨髓瘤 (MM) 的有效性. CD28对CAR T细胞的功能和在骨髓微环境中的持久性至关重要.
科学领域:
- 免疫学 免疫学 免疫学
- 在瘤学瘤学.
- 细胞疗法细胞疗法
背景情况:
- 化学抗原受体 (CAR) T细胞疗法,特别是针对B细胞成熟抗原 (BCMA),已经显示出对多发性骨髓瘤 (MM) 的承诺.
- 然而,治疗后复发率高表明需要提高CAR T细胞的疗效和在骨髓微环境 (BME) 中的持久性.
结论:
- 卡特-T细胞在体内持续的功能严重依赖于CD28信号传递.
- 使用阿巴的暂时CD28阻断可以限制CAR T细胞扩张和相关的炎症性细胞因子释放,可能减轻毒性.
- 这些发现强调了优化CD28信号传递对改善多发性骨髓瘤中CAR T细胞治疗的重要性.
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