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铜 (II) 基纳米调节器关联了cuproptosis爆发和顺序免疫细胞死亡,用于协同癌症免疫疗法

Yingli Luo^1,2, Xianyu Luo¹, Yi Ru¹

¹Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, PR China.

Biomaterials research

|June 28, 2024

概括

一种基于铜II的新型金属有机框架纳米平台 (Cu-MOF) 提供elaclomol (ES) 和铜来诱导cuproptosis并增强纤维瘤中的免疫细胞死亡 (ICD). 这种方法通过激活树突细胞和增加CD8+ T细胞透来增强抗瘤免疫力,有效抑制瘤生长.

科学领域:

生物医学工程生物医学工程
癌症研究癌症研究
免疫学免疫学免疫学

背景情况:

免疫性细胞死亡 (ICD) 对于抗瘤免疫反应至关重要,但在低免疫性瘤中具有挑战性.
细胞亡是一种新型调节细胞死亡,在这种情况下显示出增强免疫疗法的潜力.
铜离子体埃尔斯克洛莫尔 (ES) 是通过铜运输引发亡的关键.

研究的目的:

开发一个基于铜的金属有机框架 (Cu-MOF) 纳米平台,用于共同提供ES和铜.
调查这个纳米平台 (ES-Cu-MOF) 的潜力,以诱导cuproptosis和增强纤维瘤中的ICD.
评估ES-Cu-MOF在激活抗瘤免疫力和抑制瘤生长方面的治疗疗效.

主要方法:

一个基于铜的金属有机框架 (Cu-MOF) 纳米平台的制造.
在Cu-MOF中封装铜离子电离体elaclomol (ES) 进行联合交付 (ES-Cu-MOF).
在体外和体内研究评估cuproptosis诱导,ICD增强,免疫细胞激活和瘤抑制.

主要成果:

ES-Cu-MOF有效释放了Cu2+和ES,增加了线粒体ROS,并在瘤细胞中启动了cuproptosis.
连续的ICD被触发,导致显著的抗瘤免疫激活.
在瘤中积累ES-Cu-MOF,促进树突细胞激活和CD8+T细胞透,从而抑制纤维瘤的生长.

结论:

该ES-Cu-MOF纳米调节器是诱导cuproptosis和刺激ICD的一个有希望的策略.
这种方法有效地增强了癌症免疫治疗的抗瘤免疫反应.
开发的纳米平台为治疗纤维肉瘤等低免疫性瘤提供了可行的解决方案.

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