{
  "abstract": "Radiation-induced lung injury (RILI) is a common dose-limiting toxicity after radiotherapy for lung cancer, but the immunological mechanisms contributing to RILI pathogenesis remain poorly understood. Here we analyze a RILI mouse model using high-dose, restricted-field irradiation to the left lung. Flow cytometry and cytokine profiling analysis of innate lymphoid cells (ILC) reveals a radiation-induced shift from lung-resident type 2 ILCs (ILC2) toward pro-inflammatory type 1 ILCs (ILC1). Single-cell RNA-sequencing analysis of mouse lung ILC populations after radiation suggests that type I interferon (IFN) promotes radiation-induced ILC2-to-ILC1 plasticity. In vitro, IFN-β stimulation of mouse ILC2s leads to increased expression of the ILC1 markers T-bet and IFN-γ, while IFN-β stimulation of human peripheral blood mononuclear cells increases the ILC1-to-ILC2 ratio. In vivo, inhibition of type I IFN signaling attenuates lung damage after irradiation in our RILI model. Thus, our findings indicate that radiation-induced type I IFN induces ILC2-to-ILC1 plasticity to contribute to RILI pathogenesis, and suggest that targeting type I IFN signaling may be a therapeutic strategy to mitigate radiation-induced lung injury.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": "research article",
  "arxiv": null,
  "author_total": 5,
  "authors": [
    {
      "name": "Jaeho Kim",
      "orcid": "0000-0002-7773-1747"
    },
    {
      "name": "Haiqing Li",
      "orcid": "0000-0001-5583-2240"
    },
    {
      "name": "Rifat Mannan"
    },
    {
      "name": "Taylor A. Doherty"
    },
    {
      "name": "Heather M. McGee",
      "orcid": "0000-0003-3761-5087"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/4s35rr1pa5hcf.bib",
  "cited_by": 0,
  "doi": "10.1038/s41467-026-77637-3",
  "fulltext_url": "https://europepmc.org/articles/PMC13683384",
  "id": "4s35rr1pa5hcf",
  "issns": [
    "2041-1723"
  ],
  "landing_url": "https://www.nature.com/articles/s41467-026-77637-3",
  "language": "eng",
  "licence": "CC-BY-NC-ND-4.0",
  "licence_label": "CC BY-NC-ND 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by-nc-nd/4.0",
  "metadata_licence": null,
  "native_subjects": [
    [
      "openalex",
      "2403|IL-33, ST2, and ILC Pathways"
    ]
  ],
  "openalex": "W7223069388",
  "pdf_url": "https://www.nature.com/articles/s41467-026-77637-3.pdf",
  "pmcid": "PMC13683384",
  "pmid": "42901893",
  "published": "2026-10-20",
  "publisher": "Springer Science and Business Media LLC",
  "ris": "https://research.draconitic.com/paper/4s35rr1pa5hcf.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:17:39Z",
      "native_id": "10.1038/s41467-026-77637-3",
      "source": "crossref",
      "url": "https://www.nature.com/articles/s41467-026-77637-3"
    },
    {
      "first_seen": "2026-10-30T12:19:32Z",
      "native_id": "MED:42901893",
      "source": "europepmc",
      "url": "https://europepmc.org/article/MED/42901893"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "openalex:2403|IL-33, ST2, and ILC Pathways",
      "subfield": "immunology"
    }
  ],
  "title": "Type I IFN promotes ILC2-to-ILC1 plasticity in pre-clinical radiation-induced lung injury",
  "title_text": "Type I IFN promotes ILC2-to-ILC1 plasticity in pre-clinical radiation-induced lung injury",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:19:32Z",
  "url": "https://research.draconitic.com/paper/4s35rr1pa5hcf",
  "venue": "Nature Communications",
  "versions": []
}