ArticleClinical and experimental immunology2025
Intratumoral injection of R848 and poly(I:C) synergistically promoted antitumor immune responses by reprogramming macrophage polarization and activating DCs in lung cancer.
Article in Clinical and experimental immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Quaternary ammonium carbon dots for membrane perforation-immunity synergistic therapy against drug-resistant cancer metastasis.Journal of nanobiotechnology · 2026Article
- Multi-omics analysis identifies TLRscore for prognostic prediction and highlights TLR8 in macrophage-mediated antitumor immunity of lung adenocarcinoma.Frontiers in immunology · 2026Article
- EGFR-targeted affibody-polyIC polyplex kills EGFR-overexpressing cancer cells without activating the EGFR.PloS one · 2026Article
- Targeting Tumor-Associated Macrophages to Reshape the Immuno-Mechanical Landscape: Molecular Mechanisms and Therapeutic Strategies.International journal of biological sciences · 2026Review
- Engineering Innate Immunity: Recent Advances and Future Directions for CAR-NK and CAR-Macrophage Therapies in Solid Tumors.Cancers · 2025Review
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Authors and funding
11 authors.
Funding
Abstract
introductionImmunotherapy has rapidly become a primary treatment option for many lung cancer patients because of its success in treating this prevalent and deadly disease. However, the success of immunotherapy relies on overcoming the immunosuppressive tumor microenvironment, making remodeling this environment a potential strategy for lung cancer therapy. Research suggests that Toll-like receptor (TLR) agonists can impede tumor growth by promoting the conversion of tumor-associated macrophages into an M1-like state or enhancing dendritic cell development. However, there is insufficient research on the combined use of TLR agonists for treating lung cancer.
methodsIn this study, we examined how TLR agonists such as resiquimod (R848) and poly(I:C) impact lung cancer treatment when used alone or in combination. In vitro, the regulatory functions and mechanisms of R848 and poly(I:C) were analyzed in primary macrophages, RAW264.7 cells, and primary dendritic cells (DCs). Tumor treatment efficacy was assessed in vivo with a Lewis lung carcinoma (LLC) mouse model.
resultsThe combination of R848 + poly(I:C) enhances the transformation of macrophages from the M2 phenotype to the M1 phenotype by increasing inflammatory cytokine levels. The percentage of mature DCs expressing MHC-II+CD11c+ and CD86+ cells was significantly higher in the R848 + poly(I:C) group compared with the other groups. Intratumoral injection of the synergistic combination of R848 + poly(I:C) suppressed tumor growth by increasing the M1:M2 ratio in TAMs, activating DCs, and attracting CD4+ and CD8+ T cells.
conclusionR848 + poly(I:C) synergistically induces M1-like polarization of macrophages, activates DCs, and promotes effective antitumor immunity in mice with subcutaneous LLC tumors.
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