ArticleInternational journal of nanomedicine2025
Interleukin-2 Surface Displayed M1 Macrophage-Derived Extracellular Vesicles for Modulating the Tumor Microenvironment.
Article in International journal of nanomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Epigenetic profiling reveals M1 macrophages as the primary drivers of trained immunity in HSV-1 latently infected mice.PLoS pathogens · 2026Article
- A review of recent advances in exosome-mediated drug delivery for regenerative therapy and immunomodulation.Biomedical engineering online · 2026Review
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Authors and funding
4 authors.
Funding
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Abstract
Purpose: Cancer immunotherapy aims to enhance the immune system's ability to recognize and eliminate cancer cells, providing a sustained and effective immune response. However, the tumor microenvironment (TME), characterized by an abundance of tumor-associated M2 macrophages and the presence of exhausted or naïve T cells (non-effector T cells), remains a major barrier to effective immunotherapy. Herein, inflammatory M1 macrophage-derived extracellular vesicles (M1EV) were surface-modified to display interleukin-2 (M1EV_IL2), aiming to develop a multifunctional cancer immunotherapeutic agent capable of modulating both innate and adaptive immune responses. Methods: We engineered M1EV to label the surface with azide groups through metabolic glycoengineering and developed M1EV_IL2 that displayed IL-2 via bioorthogonal chemistry. M1EV_IL2 were purified by size-exclusion chromatography (SEC) and characterized through comprehensive analyses, including nanoparticle tracking analysis (NTA). In vitro macrophage repolarization and T cell activation were evaluated at the gene-expression level, followed by ex vivo assays assessing T-cell proliferation, cytokine secretion, and activation marker expression. Results: M1EV_IL2 effectively retained the intrinsic physicochemical properties of EVs while displaying IL-2 stably on its surface. It upregulated M1 macrophage markers, IL-1β and CXCL10, while downregulating the M2 macrophage marker CD206, thereby inducing M2-to-M1 macrophage repolarization. In addition, M1EV_IL2 also activated CD4 Conclusion: These results indicate that M1EV_IL2 has the potential to reshape the tumor immune landscape by simultaneously activating macrophages and T cells, thereby enhancing both innate and adaptive immune responses. Unlike conventional cancer therapies, which directly target tumor cells, M1EV_IL2 is expected to enhance immune responses, potentially mitigating adverse effects while improving therapeutic efficacy.
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