{
  "abstract": "Epidermolysis bullosa acquisita (EBA) is a mucocutaneous autoimmune blistering disorder mediated by autoantibodies against type VII collagen and subsequent splitting of the dermal-epidermal junction. Interleukin (IL)-17A promotes the production of chemokines and cytokines involved in neutrophil recruitment and activation, suggesting that IL-17A may contribute to EBA pathogenesis. We aimed to clarify the role of IL-17A in experimental EBA. Using an antibody transfer-induced EBA mouse model, we demonstrate that IL-17A promotes disease development, as pharmacological blockade of IL-17A with a neutralizing antibody ameliorated skin lesions. Gamma-delta ({gamma}{delta}) T cells were identified as the predominant cellular source of IL-17A, supported by the attenuated disease phenotype observed in {gamma}{delta}TCR-deficient mice. In addition, CD4+ T cells and neutrophils contributed to IL-17A production in experimental EBA. Mechanistically, IL-1-beta, rather than IL-23, was identified as a critical mediator of IL-17A production by {gamma}{delta} T cells in vitro, consistent with our in vivo findings. Whereas EBA severity was not reduced in IL-23p19-deficient mice, disease was markedly attenuated in IL-1R-deficient animals. Together, our study provides the first evidence that {gamma}{delta} T cell-derived IL-17A plays a pivotal role in experimental EBA and identifies a previously unrecognized IL-1{beta}/{gamma}{delta} T cell/IL-17A axis that expands current understanding of EBA immunopathogenesis.",
  "abstract_shown": true,
  "affiliations": [
    "Research Center Borstel"
  ],
  "article_type": "New results",
  "arxiv": null,
  "author_total": 10,
  "authors": [
    {
      "name": "F. Deng"
    },
    {
      "name": "S. Jukic"
    },
    {
      "name": "M. Wannick"
    },
    {
      "affs": [
        0
      ],
      "name": "A. Holscher"
    },
    {
      "name": "I. Prinz"
    },
    {
      "name": "R. J. Ludwig"
    },
    {
      "name": "E. Schmidt"
    },
    {
      "name": "X. Yu"
    },
    {
      "name": "F. Petersen"
    },
    {
      "affs": [
        0
      ],
      "name": "C. Holscher"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/4e052s7e86xwa.bib",
  "cited_by": 0,
  "doi": "10.64898/2026.11.04.763966",
  "fulltext_url": "https://www.biorxiv.org/content/10.64898/2026.11.04.763966v1.full",
  "id": "4e052s7e86xwa",
  "issns": [],
  "landing_url": "https://www.biorxiv.org/content/10.64898/2026.11.04.763966v1",
  "language": null,
  "licence": "CC-BY",
  "licence_label": "CC BY",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "biorxiv",
      "immunology"
    ]
  ],
  "openalex": null,
  "pdf_url": "https://www.biorxiv.org/content/10.64898/2026.11.04.763966v1.full.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-11-04",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/4e052s7e86xwa.ris",
  "sources": [
    {
      "first_seen": "2026-11-06T12:21:00Z",
      "native_id": "10.64898/2026.11.04.763966",
      "source": "biorxiv",
      "url": "https://www.biorxiv.org/content/10.64898/2026.11.04.763966v1"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "biorxiv:immunology",
      "subfield": "immunology"
    }
  ],
  "title": "γδ T cell-derived IL-17A aggravates experimental epidermolysis bullosa acquisita in response to IL-1β",
  "title_text": "γδ T cell-derived IL-17A aggravates experimental epidermolysis bullosa acquisita in response to IL-1β",
  "type": "preprint",
  "updated_at": "2026-11-08T00:20:56Z",
  "url": "https://research.draconitic.com/paper/4e052s7e86xwa",
  "venue": "bioRxiv",
  "versions": []
}