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通过化疗衍生的脂质纳米颗粒诱导的免疫原性细胞死亡和CD40L/Flt3L mRNA介导的树突状细胞活化增强抗肿瘤免疫力。

Enhancing antitumor immunity through chemotherapeutic-derived lipid nanoparticle-induced immunogenic cell death and CD40L/Flt3L mRNA-mediated dendritic cell activation.

作者信息

Hou Xucheng, Wang Chang, Zhong Yichen, Wang Leiming, Kang Diana D, Lubitz Gabrielle, Xue Yonger, Liu Zhengwei, Wang Siyu, Li Haoyuan, Tian Meng, Cao Dinglingge, Guo Kaiyuan, Deng Binbin, McComb David W, Marron Thomas U, Brown Brian D, Merad Miriam, Brody Joshua D, Dong Yizhou

机构信息

Marc and Jennifer Lipschultz Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Immunology and Immunotherapy, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Icahn Genomics Institute, Icahn School of Medicine at Mount Sinai, New York 10029, NY, USA; Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York 10029, NY, USA; Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Biomedical Engineering and Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.

Marc and Jennifer Lipschultz Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Immunology and Immunotherapy, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Icahn Genomics Institute, Icahn School of Medicine at Mount Sinai, New York 10029, NY, USA; Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York 10029, NY, USA; Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Biomedical Engineering and Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Division of Pharmaceutics & Pharmacology, College of Pharmacy, The Ohio State University, Columbus, OH 43210, United States.

出版信息

J Control Release. 2025 Jun 10;382:113684. doi: 10.1016/j.jconrel.2025.113684. Epub 2025 Apr 2.

Abstract

Dendritic cells (DCs) are essential for inducing effective antitumor T cell responses. However, the immunosuppressive tumor microenvironment (TME) hinders DC recruitment and maturation, facilitating tumor progression and spread. This study investigates the synergistic potential of immunogenic cell death (ICD), triggered by chemotherapeutic-derived lipid nanoparticles (LNPs), in combination with Flt3L and CD40L mRNA delivery to enhance DC mobilization and activation, reprogram the TME, and ultimately promote robust antitumor T cell responses. The optimized LNP formulation, GEM5Q7, efficiently delivered mRNA and induced ICD in melanoma cells. Intratumoral administration of GEM5Q7, encapsulating Flt3L and CD40L mRNAs, elevated pro-inflammatory cytokine and chemokine secretion, driving the infiltration and activation of cross-presenting DCs, which are critical for priming T cells. In a subcutaneous melanoma model, this approach led to significant tumor suppression and a 40 % complete response rate. This strategy holds promise for enhancing cancer immunotherapies by reprogramming the TME and inducing durable antitumor T cell immunity.

摘要

树突状细胞(DCs)对于诱导有效的抗肿瘤T细胞反应至关重要。然而,免疫抑制性肿瘤微环境(TME)会阻碍DC的募集和成熟,从而促进肿瘤的进展和扩散。本研究调查了化疗衍生的脂质纳米颗粒(LNPs)引发的免疫原性细胞死亡(ICD)与Flt3L和CD40L mRNA递送相结合的协同潜力,以增强DC的动员和激活,重新编程TME,并最终促进强大的抗肿瘤T细胞反应。优化后的LNP制剂GEM5Q7能有效地递送mRNA并在黑色素瘤细胞中诱导ICD。瘤内注射包裹Flt3L和CD40L mRNA的GEM5Q7,可提高促炎细胞因子和趋化因子的分泌,促使交叉呈递DC的浸润和激活,而交叉呈递DC对于启动T细胞至关重要。在皮下黑色素瘤模型中,这种方法导致显著的肿瘤抑制和40%的完全缓解率。该策略有望通过重新编程TME和诱导持久的抗肿瘤T细胞免疫来增强癌症免疫疗法。

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