肿瘤细胞中GPR65的失活通过巨噬细胞重塑导致抗原非依赖性CAR T细胞耐药。
GPR65 Inactivation in Tumor Cells Drives Antigen-Independent CAR T-cell Resistance via Macrophage Remodeling.
作者信息
Mavuluri Jayadev, Dhungana Yogesh, Jones Lindsay L, Bhatara Sheetal, Shi Hao, Yang Xu, Lim Song-Eun, Reyes Noemi, Chi Hongbo, Yu Jiyang, Geiger Terrence L
机构信息
Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee.
Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee.
出版信息
Cancer Discov. 2025 May 2;15(5):1018-1036. doi: 10.1158/2159-8290.CD-24-0841.
The study identifies GPR65 as an important determinant of B-cell acute lymphoblastic leukemia response to CAR T-cell therapy. Notably, GPR65 absence signals CAR T resistance. By emphasizing the therapeutic potential of targeting VEGFA or host macrophages, our study identifies routes to optimize CAR T-cell therapy outcomes in hematologic malignancies via tumor microenvironment manipulation.
该研究确定GPR65是B细胞急性淋巴细胞白血病对CAR T细胞疗法反应的重要决定因素。值得注意的是，缺乏GPR65预示着对CAR T细胞耐药。通过强调靶向VEGFA或宿主巨噬细胞的治疗潜力，我们的研究确定了通过操纵肿瘤微环境来优化血液系统恶性肿瘤中CAR T细胞治疗效果的途径。
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