决定异体 CAR T 细胞排斥与扩增的细胞和分子机制
Cellular and molecular mechanisms determining allogeneic CAR T cell rejection and expansion.
我们评估了11例接受单一批次cemacabtagene ansegedleucel(cema-cel)治疗的大B细胞淋巴瘤患者,cemacabtagene ansegedleucel是一种异体抗CD19 CAR T产品。
英文原题:CAR-NK Cells in B-cell Lymphoma: A New Frontier toward Accessible and Scalable Cellular Therapy.
在这项II期研究中,TAK-007,一种现成的表达IL-15的同种异体CD19 CAR NK细胞疗法,在经过重度预处理的B细胞淋巴瘤患者中(包括CAR-T治疗后患者)显示出令人鼓舞的缓解率、快速的治疗可及性和优异的安全性,尽管持久性有限。
在这项 II 期研究中,TAK-007 是一种现货型异基因 CD19 CAR-NK 细胞疗法,并表达 IL-15。在既往接受多线治疗的 B 细胞淋巴瘤患者(包括 CAR-T 治疗后患者)中,该疗法显示出令人鼓舞的应答率、快速可及性和良好的安全性,但疗效持久性有限。结合整合性转化研究分析,这些发现提供了 CAR-NK 生物学机制的重要线索,可指导后续优化,并推动该疗法走向更广泛的临床应用。
In this phase II study, TAK-007, an off-the-shelf allogeneic CD19 CAR NK-cell therapy expressing IL-15, demonstrates encouraging response rates, rapid treatment availability, and an excellent safety profile in heavily pretreated B-cell lymphoma, including post-CAR-T patients, albeit with limited durability. These findings, supported by integrated translational analyses, provide important mechanistic insights into CAR-NK biology that may guide future optimization and bring this approach closer to broader clinical application. See related article by Darrah et al., p. XX .
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