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:Genome-Edited T Cell Therapies.
嵌合抗原受体(CAR)T 细胞正被广泛研究用于对抗恶性肿瘤,而异基因「通用供者」CAR-T 细胞为更广泛地获得预先生产的现货型疗法提供了可能。
嵌合抗原受体(CAR)T细胞正在广泛研究用于治疗恶性肿瘤;异体“通用供者”CAR-T细胞有望扩大预先制造、现货型疗法的可及性。研究者已使用不同基因组编辑平台解决人类白细胞抗原(HLA)屏障,以制备通用CAR-T疗法;针对B细胞恶性肿瘤的早期应用已见于儿童和成人患者。近期开发的CRISPR及相关技术有望增强细胞免疫疗法,并将其拓展至更广泛的血液系统恶性肿瘤。
Chimeric antigen receptor (CAR) T-cells are widely being investigated against malignancies, and allogeneic 'universal donor' CAR-T cells offer the possibility of widened access to pre-manufactured, off-the-shelf therapies. Different genome-editing platforms have been used to address human leukocyte antigen (HLA) barriers to generate universal CAR-T cell therapy and early applications have been reported in children and adults against B cell malignancies. Recently developed Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-based systems and related technologies offer the prospect of enhanced cellular immunotherapies for a wider range of hematological malignancies.
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