ArticleFrontiers in oncology2025
IL-18-primed NK cells recruit dendritic cells and potentiate tumor therapy mediated by PD-1 blockade.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Interleukin-18 armours antitumour immune effectors.Nature reviews. Immunology · 2026Review
- Integrating single-cell and spatial transcriptomics to decipher the neuro-immune microenvironment of breast cancer brain metastasis: a key regulatory axis, prognostic model, and drug discovery.Translational cancer research · 2026Article
- IL-18 suppresses retinoblastoma growth while concomitantly inducing an inflammation-/stress-associated and immune-remodeling response.Cancer cell international · 2026Article
- Reprogramming myeloid cells and restoring T cell fitness in checkpoint inhibitor resistant melanoma patients.Biomarker research · 2026Article
- IL-18-Mediated Tumor Immune Evasion.Current issues in molecular biology · 2026Review
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4 authors.
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Abstract
The success of cancer immunotherapy depends on the effective coordination of innate and adaptive immunity. We previously reported that IL-18 potentiates the therapeutic effects of immune checkpoint inhibitors in mouse models. Here, we report that IL-18-primed natural killer (NK) cells enhanced the antitumor effects of anti-PD-1 antibodies by mobilizing type 1 conventional dendritic cells (cDC1s) to tumor sites and promoting type 1 immune responses. IL-18-primed NK cells had a premature phenotype, and expressed chemokines involved in cDC1 mobilization. In a combination treatment with IL-18 and anti-PD-1 antibody, NK cell depletion inhibited cDC1 mobilization and abrogated the therapeutic effects. Additionally, adoptive transfer of IL-18-primed NK cells induced cDC1 mobilization and enhanced the therapeutic effects of anti-PD-1 antibodies. IL-18 also increased IL-12 mRNA expression in DCs and IL-12 blood levels, and IL-12 upregulated XCL1 expression in NK cells. These results suggest that IL-18 primes NK cells and enhances the therapeutic effects of immune checkpoint inhibitors by promoting a feed-forward loop involving DCs.
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