非霍奇金淋巴瘤CAR - T细胞:同步信号、GLUT1表达和PGC1a表达的增强带来治疗的潜在临床进展

Jackson He, Yi-Jyun Chen, Zhi Feng Etan Kiang, Ly Yang
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引用次数: 0

摘要

虽然以前的恶性实体瘤治疗主要集中在手术切除和/或化疗/放疗,但现在通过监测和操纵免疫系统来对抗癌症是可行的。因此,这项工作的主要目的是假设一种潜在的联合治疗,对嵌合抗原受体T细胞有前瞻性的增强,为体内免疫受损的大鼠非霍奇金淋巴瘤模型提供预期的结果。本研究基于先前完成的研究,它提示包含Synnotch受体,它可以通过打开/关闭受体来管理T细胞衰竭和改变抗原识别,特别是调节CD19和补充CD22, CD20和CD30。除Synnotch外,本研究表明PGC1a和GLUT 1的上调可以解决肿瘤微环境中持久性差的问题,实验期间通过western blot和流式细胞术监测,此外,GM-CSF也可用于解决细胞因子释放综合征。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Non-Hodgkin Lymphoma CAR T Cells: Enhancement on Synnotch Signaling, GLUT1 expression, and PGC1a expression brings Potential Clinical Advancement in Therapy
While prior therapies for malignant solid tumors mostly focused on surgical excision and/or chemotherapy/radiotherapy, it is now feasible to combat cancers via monitoring and manipulating the immune system. Hence, the main purpose of this work is to hypothesize a potential combinational therapy with prospective enhancements to Chimeric Antigen Receptor T cells, a provision of anticipated results in vivo immune compromised Rat model with Non-Hodgkin's Lymphoma. This study, based on previously done research, it suggests the inclusion of Synnotch Receptor, which can manage T cell exhaustion and alter antigen recognition by on/off switching the receptors, particularly adjusting for CD19 and supplementary CD22, CD20, and CD30. In addition to Synnotch, this work suggests that PGC1a and GLUT 1 be upregulated to deal with the problem of poor persistence in the tumor microenvironment, monitored by western blot and flow cytometry during experiments, and in addition, with the application of GM-CSF for tackling cytokine release syndrome.
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