ArticleiScience2025
Multi-omics and functional characterization of the tumor-killing capacity of Imiquimod-activated plasmacytoid dendritic cells.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The CREM-IL-15 axis: decoding the persistence-exhaustion paradox in NK cell immunotherapy.Cancer immunology, immunotherapy : CII · 2026Review
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Authors and funding
10 authors.
Funding
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Abstract
Plasmacytoid dendritic cells (pDCs) are a subset of DCs generally associated with poor prognosis of cancer patients. However, upon TLR7/8 activation by imiquimod, pDCs have been shown to acquire tumor-killing abilities. In this study, by performing multi-omics profiling of imiquimod-stimulated murine bone marrow-derived pDCs (BM-pDCs), we identified MAPKs, JAK/STAT, and NF-κB pathways as critical mediators of the killing function. Analysis of secreted and surface markers in perturbed BM-pDCs revealed that a complex signaling network is necessary to shape the cytotoxic phenotype of imiquimod-activated BM-pDCs. While JNK inhibition reduces killing via secreted factors, p38 inhibition enhances cell-mediated killing. Instead, NF-κB inhibition boosts whereas Tyk2 deficiency reduces both cell- and secreted factors-mediated killing. Data integration identified a pDC killing gene signature with prognostic value in melanoma patients. These results will be instrumental to design further functional studies and clinical approaches to harness the anti-tumorigenic functions of pDCs, in turn improving cancer patients' outcome.
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