Key Laboratory of Biorheological Science and Technology, Ministry of Education, Chongqing University, Chongqing, 400044, PR China.
School of Life Science, Chongqing University, Chongqing, 400044, PR China.
Nat Commun. 2024 Jun 12;15(1):5035. doi: 10.1038/s41467-024-49482-9.
Radio-immunotherapy exploits the immunostimulatory features of ionizing radiation (IR) to enhance antitumor effects and offers emerging opportunities for treating invasive tumor indications such as melanoma. However, insufficient dose deposition and immunosuppressive microenvironment (TME) of solid tumors limit its efficacy. Here we report a programmable sequential therapeutic strategy based on multifunctional fusogenic liposomes (Lip@AUR-ACP-aptPD-L1) to overcome the intrinsic radio-immunotherapeutic resistance of solid tumors. Specifically, fusogenic liposomes are loaded with gold-containing Auranofin (AUR) and inserted with multivariate-gated aptamer assemblies (ACP) and PD-L1 aptamers in the lipid membrane, potentiating melanoma-targeted AUR delivery while transferring ACP onto cell surface through selective membrane fusion. AUR amplifies IR-induced immunogenic death of melanoma cells to release antigens and damage-associated molecular patterns such as adenosine triphosphate (ATP) for triggering adaptive antitumor immunity. AUR-sensitized radiotherapy also upregulates matrix metalloproteinase-2 (MMP-2) expression that combined with released ATP to activate ACP through an "and" logic operation-like process (AND-gate), thus triggering the in-situ release of engineered cytosine-phosphate-guanine aptamer-based immunoadjuvants (eCpG) for stimulating dendritic cell-mediated T cell priming. Furthermore, AUR inhibits tumor-intrinsic vascular endothelial growth factor signaling to suppress infiltration of immunosuppressive cells for fostering an anti-tumorigenic TME. This study offers an approach for solid tumor treatment in the clinics.
放射免疫疗法利用电离辐射 (IR) 的免疫刺激特性来增强抗肿瘤效果,并为治疗黑色素瘤等侵袭性肿瘤适应症提供了新的机会。然而,实体瘤中剂量沉积不足和免疫抑制的微环境 (TME) 限制了其疗效。在这里,我们报告了一种基于多功能融合脂质体 (Lip@AUR-ACP-aptPD-L1) 的可编程序贯治疗策略,以克服实体瘤固有的放射免疫治疗抵抗。具体而言,融合脂质体负载含有金的金诺芬 (AUR),并在脂质膜中插入多变量门控适体组件 (ACP) 和 PD-L1 适体,增强黑色素瘤靶向 AUR 递药,同时通过选择性膜融合将 ACP 转移到细胞表面。AUR 放大 IR 诱导的黑色素瘤细胞免疫原性死亡,以释放抗原和损伤相关分子模式(如三磷酸腺苷 (ATP)),从而触发适应性抗肿瘤免疫。AUR 敏化放疗还上调基质金属蛋白酶-2 (MMP-2) 的表达,与释放的 ATP 结合,通过类似“与”逻辑运算的过程 (AND 门) 激活 ACP,从而触发基于工程胞嘧啶-磷酸-鸟嘌呤适体的免疫佐剂 (eCpG) 的原位释放,以刺激树突状细胞介导的 T 细胞启动。此外,AUR 抑制肿瘤内在的血管内皮生长因子信号通路,抑制免疫抑制细胞的浸润,促进抗肿瘤 TME。这项研究为临床实体瘤治疗提供了一种方法。