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:CD33-CD123 IF-THEN Gating Reduces Toxicity while Enhancing the Specificity and Memory Phenotype of AML-Targeting CAR-T Cells.
我们的研究表明,在 AML 中使用靶向 CD33 和 CD123 的“IF-THEN”SynNotch 门控 CAR-T 细胞可降低肿瘤外毒性。
本研究表明,在急性髓系白血病(AML)中,采用“IF-THEN”SynNotch 门控、靶向 CD33 和 CD123 的 CAR-T 细胞可降低脱靶毒性。该策略改善了 T 细胞表型和扩增能力,同时保留造血干/祖细胞(HSPC)并减轻细胞因子释放综合征(CRS),针对现有 AML CAR-T 疗法的关键局限提出了改进方案。
Our study demonstrates the use of "IF-THEN" SynNotch-gated CAR-T cells targeting CD33 and CD123 in AML reduces off-tumor toxicity. This strategy enhances T-cell phenotype, improves expansion, preserves HSPCs, and mitigates cytokine release syndrome-addressing critical limitations of existing AML CAR-T therapies.
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