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:Chimeric Antigen Receptor T Cells in Acute Myeloid Leukemia.
高达30%接受嵌合抗原受体(CAR)T细胞治疗的急性髓系白血病(AML)患者有应答证据,尽管各试验之间异质性很高。
高达30%接受嵌合抗原受体(CAR)T细胞治疗的急性髓系白血病(AML)患者有应答证据,尽管各试验间异质性很大。这些应答很少是深度或持久的。CD123、CD33和CLL-1已成为AML中CAR T细胞最常见的靶点。针对髓系抗原的CAR T细胞会引起骨髓消融以及细胞因子释放综合征,尽管神经毒性很少见。未来的努力应集中在AML特异性抗原的发现或工程化,以及进一步增强CAR T细胞的活性。
Up to 30% of patients with acute myeloid leukemia (AML) who undergo chimeric antigen receptor (CAR) T-cell therapy have evidence of response, although trials are highly heterogeneous. These responses are rarely deep or durable. CD123, CD33, and CLL-1 have emerged as the most common targets for CAR T cells in AML. CAR T cells against myeloid antigens cause myeloablation as well as cytokine release syndrome, although neurotoxicity is rarely seen. Future efforts should focus on AML-specific antigen discovery or engineering, and on further enhancing the activity of CAR T cells.
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