细胞外囊泡衍生混合纳米平台用于放大CD47基于阻塞的癌症免疫疗法
Lu Tang1,2, Yue Yin1,2, Yuqi Cao1,2
1State Key Laboratory of Natural Medicines, Department of Pharmaceutics, School of Pharmacy, China Pharmaceutical University, Nanjing, 210009, P. R. China.
Advanced materials (Deerfield Beach, Fla.)
|June 29, 2023
概括
混合纳米微粒重编程与瘤相关的巨细胞 (TAMs),通过阻断CD47-SIRPα信号来攻击癌细胞. 这种策略增强了免疫疗法,并在临床前模型中显示出强大的抗瘤效应.
科学领域:
- 免疫学 免疫学 免疫学
- 纳米技术 纳米技术
- 在瘤学瘤学.
背景情况:
- 瘤细胞通过CD47的"不要吃我"信号逃避免疫检测,这些信号与巨细胞上的SIRPα结合.
- 将瘤相关巨细胞 (TAM) 重编程为类似M1的"吃我"表型是免疫治疗的一个关键目标.
- 阻止CD47-SIRPα相互作用对于克服瘤免疫逃避至关重要.
研究的目的:
- 开发用于向瘤细胞化和TAM表型调制的混合纳米纤维 (hEL-RS17).
- 调查RS17装饰的纳米纤维在阻断CD47-SIRPα信号传输方面的潜力.
- 评估纳米纤维递送化学疗法,光动力学疗法和免疫调节的联合治疗效果.
主要方法:
- 从M1巨细胞外囊泡中工程混合纳米囊 (hEL-RS17) 并用RS17来装饰它们.
- 在hEL-RS17中同时封装shikonin (化疗),IR820 (光敏感剂) 和polymetformin (免疫调节剂).
- 在激光照射下评估纳米粒子向,TAM表型重塑和4T1乳腺瘤和B16F10黑色素瘤模型中的抗瘤疗效.
主要成果:
- hEL-RS17纳米纤维积极向瘤细胞,并有效地重塑TAM,使其成为类似M1的表型.
- 通过RS17阻断CD47,促进了TAM透和瘤细胞的化.
- 联合治疗 (SPI@hEL-RS17) 显示显著抑制了原发性瘤生长,减少了肺转移,并防止了瘤复发.
结论:
- 设计的SPI@hEL-RS17纳米粒子有效地阻断CD47-SIRPα信号传递,增强TAM介导的细胞分裂,并提供多模式的治疗有效载荷.
- 这种组合策略表现出强大且协同作用的抗瘤疗效,突出了其在推进基于CD47阻断的癌症免疫疗法的潜力.
- 纳米纤维平台通过克服免疫逃避和结合多种治疗方式来治疗各种癌症类型,显示出有前途的希望.
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