嵌合抗原受体
生物
细胞生物学
趋化性
癌症研究
受体
NK-92
白细胞介素21
白细胞介素12
渗透(HVAC)
免疫疗法
自然杀伤细胞
癌细胞
肿瘤微环境
癌症免疫疗法
抗原
淋巴因子激活杀伤细胞
自然杀伤性T细胞
化学
免疫系统
过继性细胞移植
T细胞
免疫学
细胞
抗原提呈细胞
造血
淋巴细胞
细胞培养
细胞疗法
白细胞介素2受体
获得性免疫系统
体外
体内
细胞毒性T细胞
作者
Young‐Min Kim,Min K. Tsai,Chang Sun,Olivia Laveroni,Reece Villarin Akana,Kristen R. Frombach,Livnat Jerby
标识
DOI:10.1038/s41590-026-02473-y
摘要
Natural killer (NK) cells and T cells need to infiltrate solid tumors to eradicate them. Here we show programmable mechanisms that can mobilize NK and T cells to solid tumors using metabolite-sensing receptors. In vivo and in vitro CRISPR activation screens using NK-92 cells identified GPR183, GPR84, GPR34 and GPR18 as top enhancers of infiltration and chemotaxis to breast and ovarian cancers. While endogenously expressed in restricted cellular contexts, expressing these receptors in NK and T cells drives migration to factors released by cancer cells and alters the NK cell transcriptome in a ligand-dependent manner. Expressing GPR183 in NK, chimeric antigen receptor (CAR) NK and CAR T cells increased tumor infiltration and control. Likewise, expressing GPR183 in mouse T cells increased tumor eradication in immunocompetent mice. These data show that metabolite sensing can be rewired to obtain biochemically guided spatially targeted cells, creating new possibilities for therapeutic intervention. Here the authors use CRISPR activation screens to identify metabolite-sensing receptors that affect lymphocyte targeting and infiltration of tumors and engineer CAR T and CAR NK cells with these receptors to enhance solid tumor killing in mice.
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