Jurkat细胞
转导(生物物理学)
生物
嵌合抗原受体
T细胞受体
基因
T细胞
重组DNA
病毒
原电池
细胞生物学
分子生物学
HEK 293细胞
病毒学
基因敲除
细胞培养
抗原
链霉菌
肽库
融合蛋白
肽
细胞
计算生物学
遗传增强
抗原提呈细胞
基因组编辑
基因剔除小鼠
细胞毒性T细胞
遗传学
基因工程
作者
Mi Leng,Chunmei Gan,Zhaoyue Zheng,S N He,Ying Liu,L. P. Zhou,R. Holland Cheng,Jiao Zhou,Lin Xiao,Jingya Ye,Zhian Chen,Xu Lz,C. Alexander Valencia,Hoi Yee Chow,Yan Zhang,Biao Dong
标识
DOI:10.1177/10430342261424779
摘要
Chimeric antigen receptor T (CAR-T) cells, created by gene editing systems along with recombinant adeno-associated virus (rAAV), provide a promising strategy for treating leukemia. rAAVs serve as a safe and effective donor template for homology-directed repair because they can avoid integrating into the host genome. However, only a few AAV serotypes can efficiently transduce human primary T cells at low multiplicities of infection (MOIs) with high packaging efficiency. To address this problem, variants derived from an AAV2 peptide library were screened in Jurkat cells and later validated in primary T cells. A high-ranking sequence identified outside the VR-VIII region, NNSKLTV, was discovered after three rounds of selection and was named Tot3. Tot3 demonstrated transduction efficiency similar to AAV2, but at a 27-fold lower MOI. In addition, Tot3 exhibited greater packaging efficiency and reduced thermal stability. Simultaneously, programmed cell death protein 1 (PD-1) knockout and CAR overexpression were achieved in human primary T cells using Tot3, with knockout and knock-in efficiencies reaching up to 70% and 55%, respectively. These CAR-T cells demonstrated significantly enhanced antitumor activity and increased survival times in a mouse model of diffuse B cell lymphoma.
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