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使用纳米脂质体调节瘤外体和纤维细胞表型可以增加癌症免疫疗法

May S Freag^1,2, Mostafa T Mohammed^1,3, Arpita Kulkarni^1,4

¹Division of Engineering in Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

Science advances

|February 28, 2024

概括

这项研究表明,阻断癌细胞外体和纤维细胞生长因子受体 (FGFR) 信号传输可以使癌症相关纤维细胞 (CAF) 正常化. 这种方法增强了T细胞的透,并提高了免疫治疗对肺癌的有效性.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
纳米技术纳米技术

背景情况:

癌细胞通过涉及外体和信号通路的两步过程将纤维细胞重编程为癌症相关纤维细胞 (CAF).
CAFs创造了一个免疫抑制的瘤微环境,阻碍了有效的癌症免疫治疗.
向CAF激活是增强抗癌治疗的潜在策略.

研究的目的:

研究一种双向纳米脂质体策略,以抑制CAF激活并提高免疫疗法的疗效.
阻断癌细胞对外体介导纤维细胞的激活.
通过抑制FGFR-Wnt/β-catenin信号传递,将被激活的CAF逆转为静止的纤维细胞.

主要方法:

开发针对癌细胞的纳米脂质体,以抑制外体细胞生物发生和释放.
开发针对CAF的纳米脂质体,以阻止FGFR-Wnt/β-catenin信号传递.
在具有免疫能力的肺癌携带小鼠中同时使用这两种纳米脂质体.

主要成果:

针对癌细胞的纳米脂质体成功地阻断了纤维细胞分化到CAF.
针对CAF的纳米脂质体逆转了激活的CAF,变成了静止的纤维细胞.
联合纳米脂酶体疗法显著增加了细胞毒性T细胞的透,并增强了αPD-L1免疫疗法的抗瘤疗效.

结论:

同时抑制瘤外体介导纤维细胞激活和FGFR-Wnt/β-catenin信号传递是一种增强癌症免疫疗法的有希望的方法.
这种双重准策略使瘤微环境正常化,并增强抗瘤免疫反应.
这些发现支持开发针对肺癌的基于纳米医学的新型组合疗法.

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