{
  "abstract": "Group 2 innate lymphoid cells (ILC2s) contribute to type 2 asthma through rapid production of interleukin-5 and interleukin-13, but the inhibitory pathways that restrain pathogenic ILC2 activity remain incompletely defined. Most evidence for programmed cell death protein 1 (PD-1)-mediated inhibition of ILC2s comes from murine models, humanized mice, and stimulated or expanded human cells; cell-resolved expression and functional engagement of PD-1 have not been established in freshly isolated airway ILC2s from well-characterized asthma cohorts. In available experimental systems, PD-1 engagement suppresses ILC2 proliferation and cytokine production, whereas programmed death-ligand 1 (PD-L1) displayed by ILC2s can act outwardly on PD-1-positive CD4-positive T cells. Programmed death-ligand 2 (PD-L2) can inhibit isolated ILC2s through PD-1, but its whole-lung effects also involve dendritic-cell IL-12 regulation and RGMb-dependent respiratory tolerance. Interpretation therefore depends on the ligand-bearing and responding cells, ligand form, tissue compartment, disease stage, and asthma endotype. This review examines cell-intrinsic PD-1 signaling, ligand-specific cellular interactions, immunometabolic regulation, and translational constraints. The current evidence supports preclinical investigation rather than clinical readiness; direct validation in human airway ILC2s, definition of receptor-proximal signaling, and a predictive biomarker are prerequisites for therapeutic development.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": "Review",
  "arxiv": null,
  "author_total": 4,
  "authors": [
    {
      "name": "Liu Ma"
    },
    {
      "name": "Mingrong Zhang"
    },
    {
      "name": "Shengdong Gou"
    },
    {
      "name": "Qifu He"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/91fgg6yr8t8x0.bib",
  "cited_by": 0,
  "doi": "10.3389/fphar.2026.1988503",
  "fulltext_url": null,
  "id": "91fgg6yr8t8x0",
  "issns": [
    "1663-9812"
  ],
  "landing_url": "https://www.frontiersin.org/articles/10.3389/fphar.2026.1988503",
  "language": null,
  "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": [
    [
      "feed-journal",
      "medicine/pharmacology-toxicology"
    ]
  ],
  "openalex": null,
  "pdf_url": null,
  "pmcid": null,
  "pmid": null,
  "published": "2026-11-04",
  "publisher": "Frontiers Media SA",
  "ris": "https://research.draconitic.com/paper/91fgg6yr8t8x0.ris",
  "sources": [
    {
      "first_seen": "2026-11-04T12:20:50Z",
      "native_id": "10.3389/fphar.2026.1988503",
      "source": "feed-frontiers",
      "url": "https://www.frontiersin.org/articles/10.3389/fphar.2026.1988503"
    },
    {
      "first_seen": "2026-11-05T00:21:10Z",
      "native_id": "10.3389/fphar.2026.1988503",
      "source": "crossref",
      "url": "https://www.frontiersin.org/articles/10.3389/fphar.2026.1988503/full"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "feed-journal:medicine/pharmacology-toxicology",
      "subfield": "pharmacology-toxicology"
    }
  ],
  "title": "PD-1 and its ligands in ILC2-mediated airway inflammation in asthma: context-dependent mechanisms and therapeutic implications",
  "title_text": "PD-1 and its ligands in ILC2-mediated airway inflammation in asthma: context-dependent mechanisms and therapeutic implications",
  "type": "peer-reviewed",
  "updated_at": "2026-11-06T00:21:25Z",
  "url": "https://research.draconitic.com/paper/91fgg6yr8t8x0",
  "venue": "Frontiers in Pharmacology",
  "versions": []
}