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对抗BCMA和CD229的二基斯特龙CAR T细胞有效控制骨髓瘤,即使BCMA表达有限,也有效控制骨髓瘤
Luis Gerardo Rodríguez-Lobato1,2,3, Oriol Cardús2,3, Joan Mañé-Pujol2,3
1Amyloidosis and Multiple Myeloma Unit, Department of Hematology, Hospital Clínic of Barcelona, Barcelona, Spain.
Cancer immunology research
|June 27, 2025
概括
新的仿真抗原受体 (CAR) T细胞疗法单独针对CD229或与BCMA一起,以克服多发性骨髓瘤的耐药性,在临床前模型中显示出希望.
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:
- 抗B细胞成熟抗原 (BCMA) 嵌合抗原受体 (CAR) T细胞疗法在复发性/耐药性多发性髓瘤中显示出高响应率.
- 治疗失败通常是由于BCMA损失或恶性血细胞表达减少.
- 创新的治疗目标和策略对于改善患者的治疗结果至关重要.
研究的目的:
- 开发和验证针对CD229和/或BCMA的新型CAR T细胞疗法.
- 在临床前多发性骨髓瘤模型中评估单特异性和双特异性CAR T细胞的疗效.
- 评估针对BCMA阴性或低表达多发性髓瘤的CD229的治疗潜力.
主要方法:
- 开发单特异性抗CD229 CAR T细胞和双特异性抗CD229/BCMA CAR T细胞.
- 在体外和体内评估使用NOD.Cg-Prkdcscid Il2rdtm1Wjl/SzJ小鼠模型.
- 在同质,异质和BCMA删除/低表达多发性髓瘤的模型中评估疗效.
主要成果:
- 单特异性抗CD229 CAR T细胞对具有不同BCMA表达的多发性骨髓瘤模型有效.
- 双抗CD229/BCMA CAR T细胞在具有同质BCMA表达的模型和具有BCMA删除或减少表达的模型中显示出有效性.
- 观察到有限的点外瘤毒性,没有兄弟杀伤,但对非激活的T细胞进行了一些消除. 在某些情况下,免疫压力导致CD229抗原损失.
结论:
- CD229是多发性骨髓瘤的可行的免疫治疗点.
- 结合CD229和BCMA目标,提供了一种有前途的策略来克服与BCMA相关的抗药性.
- 这些发现支持对多发性骨髓瘤的CD229向CAR-T细胞的临床研究,特别是在BCMA表达减少的情况下.
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