嵌合抗原受体
癌症研究
免疫系统
肿瘤微环境
T细胞
免疫疗法
分泌物
抗体
体内
抗原
化学
免疫学
免疫抑制
癌症免疫疗法
细胞疗法
生物
髓系细胞
血管生成
医学
癌细胞
髓源性抑制细胞
癌症
受体
细胞毒性
肿瘤坏死因子α
细胞
药理学
细胞毒性T细胞
细胞培养
细胞生物学
内生
脂肪组织
单克隆抗体
细胞生长
作者
Torahito A. Gao,Ryan Shih,Justin Clubb,Shao-Hsi Hung,Tanya Singh,Laura B. James‐Allan,Gabriella DiBernardo,Amanda Shafer,Amber Bouren,Melanie Ayala Ceja,Sophie Ong,Andréa B. Ball,Ajit S. Divakaruni,Sanaz Memarzadeh,Wu Han-Chung,Yvonne Y. Chen
标识
DOI:10.1126/scitranslmed.adw9286
摘要
Chimeric antigen receptor (CAR) T cell therapy has shown limited efficacy against solid tumors, which often reside in highly immunosuppressive tumor microenvironments (TMEs). TMEs can be highly abundant in vascular endothelial growth factor A (VEGF), which contributes to immunosuppression and abnormal tumor vasculature. Here, we found that CAR T cells engineered to secrete an anti-VEGF single-chain variable fragment (CAR-αVEGF T cells) achieved superior antitumor efficacy against multiple in vivo models of ovarian cancer and glioma, outperforming conventional CAR T cells with and without combination anti-VEGF antibody therapy. Microscopy, flow cytometry, and transcriptomic analyses revealed that armoring the CAR T cells with anti-VEGF single-chain variable fragments enhanced their activation and mitochondrial fitness and enriched immune-stimulatory signatures among endogenous immune cells in the tumor-bearing brain. Moreover, CAR-αVEGF T cells circumvented multiple detrimental effects associated with on-target CAR T cell therapy, including infiltration of suppressive myeloid cells, exaggerated vasculature abnormalities, and hypoxia. Together, our results provide rationale for the clinical translation of CAR-αVEGF T cells as a safe and potent therapy for solid tumors characterized by elevated VEGF.
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