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:Targeted CD7 CAR T-cells for treatment of T-Lymphocyte leukemia and lymphoma and acute myeloid leukemia: recent advances.
CD7在T细胞急性淋巴细胞白血病(T-ALL)和T淋巴瘤中的高表达已引起研究者的广泛关注。
CD7在T细胞急性淋巴细胞白血病(T-ALL)和T淋巴瘤中的高表达已引起研究者的广泛关注。然而,由于CD7嵌合抗原受体(CAR)T细胞会发生自相残杀,CD7 CAR T细胞会出现耗竭表型,从而损害CAR T细胞的效果。过去几年,CD7靶向CAR T细胞治疗已取得重大突破。基因编辑、蛋白阻断剂及其他方法的出现,有效克服了传统CD7 CAR T细胞方法的不良影响。本综述结合第64届美国血液学会(ASH)年会的最新进展,总结了近年来CD7 CAR T细胞代次和临床试验方面的重要成就。
The high expression of CD7 targets in T-cell acute lymphoblastic leukemia (T-ALL) and T-lymphoma has attracted considerable attention from researchers. However, because CD7 chimeric antigen receptor (CAR) T-cells undergo fratricide, CD7 CAR T-cells develop an exhaustion phenotype that impairs the effect of CAR T-cells. There have been significant breakthroughs in CD7-targeted CAR T-cell therapy in the past few years. The advent of gene editing, protein blockers, and other approaches has effectively overcome the adverse effects of conventional methods of CD7 CAR T-cells. This review, in conjunction with recent advances in the 64 th annual meeting of the American Society of Hematology (ASH), provides a summary of the meaningful achievements in CD7 CAR T-cell generations and clinical trials over the last few years.
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