ArticleJournal for immunotherapy of cancer2025
Inhibition of osteosarcoma lung metastases by β-glucan and CD40 agonist is mediated by activation of macrophages and NK cells.
Article in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- DAMPs, PAMPs, and Alarmins: From Mechanism to Therapy.MedComm · 2026Review
- PCGF1-mediated bivalent promoter remodeling enables NK cell immune evasion in non-small cell lung cancer.Cell death & disease · 2026Article
- Dynamic immune state transitions and metastatic niche remodelling drive osteosarcoma evolution as a barrier-restricted immune-cold ecosystem.Frontiers in immunology · 2026Review
- Dynamic changes in peripheral blood lymphocyte subsets predict the efficacy and prognosis of immune checkpoint inhibitors in metastatic osteosarcoma.Frontiers in immunology · 2026Article
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3 authors.
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Abstract
backgroundOsteosarcoma (OS) lung metastases remain a significant therapeutic challenge. Innate immune activation is a promising therapeutic approach. Innate immune agonists can modulate the tumor immune microenvironment and improve therapeutic response.
methodsUsing an experimental syngeneic OS lung metastasis BALB/c mouse model with K7M3-luc OS cells, we evaluated the antitumor effects of yeast-derived particulate β-glucan in prevention and therapeutic settings. We then assessed whether the CD40 agonist (CD40a) in combination with β-glucan increased therapeutic response in two different immune-competent mouse models of OS lung tumor burden.
resultsIn the pretreatment settings, mice treated with β-glucan prior to OS cell infusion developed significantly fewer lung tumor burdens and had increased survival. Pretreatment with β-glucan prevented tumor cell seeding in the lungs. In tumor-bearing mice, β-glucan treatment significantly suppressed tumor growth and prolonged overall survival. β-glucan treatment increased activated pro-inflammatory M1-like macrophages and natural killer (NK) cells secreting interferon-γ and granzyme B in the lungs. Depletion studies showed that the antitumor effect of β-glucan was dependent on macrophages and NK cells. Additionally, β-glucan treatment also induced myelopoiesis in the bone marrow. The therapeutic benefit of β-glucan was further augmented when combined with CD40a. Combination therapy significantly increased the infiltration of activated macrophages, including tumor necrosis factor-α secreting macrophages, and NK cells into the lungs compared with monotherapy. Bulk RNA sequencing of lung tissue revealed that the combination treatment group exhibited enhanced activation of antitumor innate immune pathways.
conclusionsCollectively, our findings demonstrate the antitumor activity of β-glucan against OS lung tumor burden, that combining β-glucan and CD40a increases therapeutic activity, and that this activity is mediated by activation of innate immunity (macrophages and NK cells).
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