{
  "abstract": "Plasmacytoid dendritic cells (pDCs) are specialized immune cells best known for their ability to produce large amounts of type I interferons (IFN-I) upon nucleic acid sensing through endosomal Toll-like receptors (TLR)-7/8 and 9. In tumors, the accumulation of nucleic acids (NAs) deriving from extensive cancer cell death would be expected to activate pDCs and induce IFN-I–mediated anti-tumor responses. However, tumor-infiltrating pDCs typically exhibit impaired IFN-I production and instead acquire immunosuppressive properties, revealing a paradox between NAs availability and pDC function within the tumor microenvironment (TME). In this review, we examine current knowledge and explore the mechanisms that may constrain IFN-I responses by pDCs, including chronic stimulation, alterations in TLR signaling and limited accessibility of tumor-derived NAs. We discuss key open questions regarding how tumor-associated signals may impair pDC responsiveness and contribute to their dysfunction, the nature and immunostimulatory potential of tumor-derived NAs, and their intracellular delivery. By highlighting these unresolved questions, we propose conceptual frameworks to better understand pDC biology in cancer and identify strategies to restore their IFN-I–mediated antitumor functions.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": null,
  "arxiv": null,
  "author_total": 6,
  "authors": [
    {
      "name": "Aliki Vasilakou"
    },
    {
      "name": "Séverine Loizon"
    },
    {
      "name": "Maxime Dubois"
    },
    {
      "name": "Paôline Laurent"
    },
    {
      "name": "Vanja Sisirak"
    },
    {
      "name": "Dorothée Duluc"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/2fb0eczce77k7.bib",
  "cited_by": 1,
  "doi": "10.3389/fimmu.2026.1847012",
  "fulltext_url": null,
  "id": "2fb0eczce77k7",
  "issns": [
    "1664-3224",
    "1664-3224"
  ],
  "landing_url": "https://u-bordeaux.hal.science/hal-05737698v1",
  "language": "en",
  "licence": "CC-BY-4.0",
  "licence_label": "CC BY 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "hal",
      "0.sdv"
    ],
    [
      "hal",
      "1.sdv.imm"
    ],
    [
      "openalex",
      "2403|Immunotherapy and Immune Responses"
    ]
  ],
  "openalex": "W7167058018",
  "pdf_url": "https://u-bordeaux.hal.science/hal-05737698/document",
  "pmcid": null,
  "pmid": null,
  "published": "2026-07-02",
  "publisher": "Frontiers",
  "ris": "https://research.draconitic.com/paper/2fb0eczce77k7.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:17:27Z",
      "native_id": "hal-05737698",
      "source": "hal",
      "url": "https://u-bordeaux.hal.science/hal-05737698v1"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "hal:1.sdv.imm",
      "subfield": "immunology"
    }
  ],
  "title": "The plasmacytoid dendritic cell paradox in cancer: impaired type I interferon responses in a nucleic acid–rich tumor microenvironment",
  "title_text": "The plasmacytoid dendritic cell paradox in cancer: impaired type I interferon responses in a nucleic acid–rich tumor microenvironment",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:17:27Z",
  "url": "https://research.draconitic.com/paper/2fb0eczce77k7",
  "venue": "Frontiers in Immunology",
  "versions": []
}