RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Generation of a homozygous TIGIT gene knockout (TIGIT(-/-)) human iPSC line (MUSIi001-A-3) using CRISPR/Cas9 system.
Generation of a homozygous TIGIT gene knockout (TIGIT(-/-)) human iPSC line (MUSIi001-A-3) using CRISPR/Cas9 system.
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实体瘤的过继细胞疗法涉及增强并回输免疫细胞以靶向肿瘤细胞。诱导多能干细胞技术的进步使得能够生成用于ACT的T细胞和NK细胞等免疫细胞产品。然而,TIGIT等抑制性受体的表达可能限制这些免疫效应细胞的功能。在本研究中,我们构建了纯合TIGIT基因敲除iPSC系,以期阻止抑制性信号传导和耗竭,从而为细胞免疫治疗应用创建强效的“现货型”免疫细胞产品。这种方法可能为抗击实体瘤开辟新的前沿。
Adoptive cell therapy for solid cancers involves enhancing and reinfusing immune cells to target tumor cells. The advancement of induced pluripotent stem cell technology enables the generation of immune cell products like T and NK cells for ACT.
However, the expression of inhibitory receptors, such as TIGIT, may limit the functionality of these immune effector cells. In this study, we generated a homozygousTIGITgene knockout iPSC line to potentially prevent inhibitory signaling and exhaustion, thereby creating potent "off-the-shelf" immune cell products for cellular immunotherapy applications. This approach could offer a new frontier in the fight against solid tumors.
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