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-ving a Path: Metalloprotease-Engineered CAR T Cells Tunnel through Solid Tumors.
克服肿瘤微环境的物理屏障仍是嵌合抗原受体(CAR)T 细胞疗法治疗实体瘤的主要障碍。
克服肿瘤微环境的物理屏障仍是CAR-T细胞疗法治疗实体瘤的主要障碍。本期Van Pelt及其同事的研究显示,对靶向GD2的CAR-T细胞进行工程化改造,使其表达基质金属蛋白酶7和增强型骨桥蛋白,可提高其浸润富含细胞外基质肿瘤的能力。这些改造在临床前模型中增强了功能,且未增加脱靶毒性。研究结果凸显了一种有前景策略:设计具有细胞外基质重塑能力的CAR-T细胞。相关论文见Van Pelt等,第1732页。
Overcoming the physical barriers of the tumor microenvironment remains a major obstacle for chimeric antigen receptor (CAR) T-cell therapy in solid tumors. In this issue, Van Pelt and colleagues show that engineering GD2-targeting CAR T cells to express matrix metalloproteinase 7 and osteopontin-b enhances their ability to infiltrate tumors rich in extracellular matrix. These modifications improve functionality in preclinical models without increasing off-target toxicity. The findings highlight a promising strategy to design CAR T cells with extracellular matrix-remodeling capabilities. See related article by Van Pelt et al., p. 1732.
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