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<p>The tumour microenvironment (TME) causes mitochondrial dysfunction in resident dendritic cells (DCs), resulting in inadequate antigen presentation and weak T cell priming. Herein, we identify hypoxia as a key factor for causing pathological mitochondrial fission in tumour-associated DCs, and develop a plant vesicle-DC chimera to relieve hypoxia-induced mitochondrial dysfunction for enhancing cancer immunotherapy. The biohybrid chimera is fabricated by loading algae-derived nanovesicles (ANVs) with genetically engineered CCR2 overexpressing-DCs. The CCR2-DC-ANVs target tumour by leveraging the C-C motif chemokine ligand 2 (CCL2) in tumours. Upon light exposure, the ANVs produce oxygen and NADPH to resolve hypoxic and oxidative stress, which reverse pathological mitochondrial fission in DCs. Mitochondrial network restoration alleviates endoplasmic reticulum stress, reduces lipid droplet accumulation, and initiates metabolic reprogramming to enhance antigen presentation and T cell priming of CCR2-DC-ANVs in the TME. The biohybrid chimera enhances therapeutic efficiency in humanized mouse models of breast cancer in female mice without requiring external tumour antigens. This approach highlights a cross-species chimera for next-generation DC therapy, and provides the basis for a nanobiotechnology platform to facilitate organelle medicine by combining photosynthesis with immunotherapy.</p>

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A plant vesicle-dendritic cell chimera for enhancing cancer immunotherapy

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月28日

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  • Wenzhe Yi,
  • Xindi Qian,
  • Wenlu Yan,
  • Dan Yan,
  • Zhiwen Zhao,
  • Fang Sun,
  • Qi Zhao,
  • Dangge Wang,
  • Yaping Li

摘要

The tumour microenvironment (TME) causes mitochondrial dysfunction in resident dendritic cells (DCs), resulting in inadequate antigen presentation and weak T cell priming. Herein, we identify hypoxia as a key factor for causing pathological mitochondrial fission in tumour-associated DCs, and develop a plant vesicle-DC chimera to relieve hypoxia-induced mitochondrial dysfunction for enhancing cancer immunotherapy. The biohybrid chimera is fabricated by loading algae-derived nanovesicles (ANVs) with genetically engineered CCR2 overexpressing-DCs. The CCR2-DC-ANVs target tumour by leveraging the C-C motif chemokine ligand 2 (CCL2) in tumours. Upon light exposure, the ANVs produce oxygen and NADPH to resolve hypoxic and oxidative stress, which reverse pathological mitochondrial fission in DCs. Mitochondrial network restoration alleviates endoplasmic reticulum stress, reduces lipid droplet accumulation, and initiates metabolic reprogramming to enhance antigen presentation and T cell priming of CCR2-DC-ANVs in the TME. The biohybrid chimera enhances therapeutic efficiency in humanized mouse models of breast cancer in female mice without requiring external tumour antigens. This approach highlights a cross-species chimera for next-generation DC therapy, and provides the basis for a nanobiotechnology platform to facilitate organelle medicine by combining photosynthesis with immunotherapy.