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:Lowering mTORC1 Drives CAR T-Cells Home in Acute Myeloid Leukemia.
迄今为止,细胞疗法在急性髓系白血病(AML)中显示出的疗效有限。
迄今为止,细胞疗法在急性髓系白血病(AML)中显示出有限的疗效。一项近期研究表明,mTOR复合物1激活下调CXCR4,从而减少靶向EpCAM的嵌合抗原受体(CAR)T细胞在AML中的骨髓浸润。在IL2介导的体外扩增过程中,通过联合使用mTOR抑制剂阻断mTOR信号通路,可上调CXCR4,并增强CAR T细胞的骨髓迁移及对AML的清除能力。参见Nian等人发表于第6026页的相关文章。
Cellular therapies have demonstrated limited efficacy thus far in acute myeloid leukemia (AML). A recent study shows that mTOR complex 1 activation downregulated CXCR4 reducing marrow infiltration of EpCAM-targeting chimeric antigen receptor (CAR) T-cells in AML. Abrogating mTOR signaling by cotreatment with mTOR inhibitors during IL2-mediated ex vivo expansion upregulated CXCR4 and bolstered bone marrow migration and AML elimination by CAR T-cells. See related article by Nian et al., p. 6026 .
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