{
  "abstract": "Background: While immune dysfunction is recognized as pivotal in biliary atresia (BA) pathogenesis, comprehensive characterization of disease-specific immune cell subtypes and stromal components remains incomplete. This study aims to define the altered hepatic immune-stromal landscape and aberrant intercellular communication networks associated with BA progression using single-cell transcriptomics.\n\nMethods: We performed single-cell RNA sequencing (scRNA-seq) on BA liver tissues to profile immune and stromal cell populations. Cellular subclustering, differential gene expression, pathway enrichment, and cell-cell communication analyses were employed to identify potential pathogenic drivers and predicted possible signaling networks. Multiplex immunofluorescence staining was used to verify receptor-ligand interaction in BA liver.\n\nResults: BA livers exhibited profound expansion of pro-inflammatory neutrophil subsets - Neutrophils with interferon-stimulated genes (Neu_ISG), Aged neutrophils (Neu_Aged) - with transcriptional signatures suggestive of enhanced reactive oxygen species (ROS) production, extracellular matrix (ECM) modulation, and cytokine activity. Concurrent cytotoxic/immunoregulatory lymphocyte populations - Effector memory CD4⁺ T Cell (CD4⁺ TEM), Tregs, cytotoxic NK cells- showed upregulated inflammatory and oxidative stress pathways. Periportal and lymphatic liver endothelial cells (LECs) demonstrated significant perturbations. Central venous LECs displayed signatures of oxidative stress and dysregulated proliferation/migration. Cell-cell communication analysis highlighted a possibly dominant “CXCL12-CXCR4” axis mediating neutrophil recruitment across endothelia, NK&T/B, and myeloid cells. Enhanced “MIF-CD74/CXCR4” signaling between endothelia and immune cells, “VEGFB-VEGFR1” interactions between hepatocyte-cholangiocyte compartments and central venous/periportal endothelia were observed, suggesting that these interactions are associated with BA progression.\n\nConclusion: Our scRNA-seq atlas uncovers coordinated innate/adaptive immune responses and endothelial-stromal dysfunction that shape a hepatic niche in BA associated with ROS, unchecked inflammation, and fibrotic remodeling. Key cellular and molecular contributors include pathogenic neutrophils, cytotoxic lymphocytes, and injured endothelia, which interact via “CXCL12-CXCR4” and “VEGFB-VEGFR1” signaling axes. These findings from the present exploratory study point to potential novel therapeutic targets (e.g., neutrophil subsets, chemokine pathways) for mitigating BA pathogenesis.",
  "abstract_shown": true,
  "affiliations": [
    "Department of General Surgery, Capital Center for Children’s Health, Capital Medical University, Capital Institute of Pediatrics , ,",
    "Department of Biochemistry and Immunology, Capital Center for Children’s Health, Capital Medical University, Capital Institute of Pediatrics , ,",
    "Department of Pathology, Heilongjiang Hospital of Beijing Children’s Hospital, Capital Medical University , ,",
    "Department of Science and Technology, Capital Center for Children’s Health, Capital Medical University, Capital Institute of Pediatrics , ,"
  ],
  "article_type": "research article",
  "arxiv": null,
  "author_total": 9,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Xuelai Liu"
    },
    {
      "affs": [
        1
      ],
      "name": "Zhuo Liu"
    },
    {
      "affs": [
        2
      ],
      "name": "Huan Wang"
    },
    {
      "affs": [
        0
      ],
      "name": "Yuqiang Chen"
    },
    {
      "affs": [
        0
      ],
      "name": "Mao Ye"
    },
    {
      "affs": [
        0
      ],
      "name": "Xu Li"
    },
    {
      "affs": [
        0
      ],
      "name": "Yuanyuan Geng"
    },
    {
      "affs": [
        3
      ],
      "name": "Xiaoyun Cui"
    },
    {
      "affs": [
        1
      ],
      "name": "Feng He"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/c2qk87f4dytay.bib",
  "cited_by": 0,
  "doi": "10.3389/fped.2026.1995199",
  "fulltext_url": "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13719468/?tool=EBI",
  "id": "c2qk87f4dytay",
  "issns": [
    "2296-2360"
  ],
  "landing_url": "https://europepmc.org/article/PMC/PMC13719468",
  "language": "eng",
  "licence": "CC-BY",
  "licence_label": "CC BY",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "heading",
      "Original Research"
    ],
    [
      "openalex",
      "2746|Pediatric Hepatobiliary Diseases and Treatments"
    ]
  ],
  "openalex": "W7222455864",
  "pdf_url": "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13719468/pdf/?tool=EBI",
  "pmcid": "PMC13719468",
  "pmid": "42964246",
  "published": "2026-10-16",
  "publisher": "Frontiers Media SA",
  "ris": "https://research.draconitic.com/paper/c2qk87f4dytay.ris",
  "sources": [
    {
      "first_seen": "2026-10-31T12:21:36Z",
      "native_id": "PMC:PMC13719468",
      "source": "europepmc",
      "url": "https://europepmc.org/article/PMC/PMC13719468"
    },
    {
      "first_seen": "2026-11-02T12:23:25Z",
      "native_id": "PMC13719468",
      "source": "pmc",
      "url": "https://doi.org/10.3389/fped.2026.1995199"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "openalex:2746|Pediatric Hepatobiliary Diseases and Treatments",
      "subfield": "surgery"
    }
  ],
  "title": "Single-cell transcriptome atlas revealed liver immune features in biliary atresia",
  "title_text": "Single-cell transcriptome atlas revealed liver immune features in biliary atresia",
  "type": "peer-reviewed",
  "updated_at": "2026-11-03T12:20:31Z",
  "url": "https://research.draconitic.com/paper/c2qk87f4dytay",
  "venue": "Frontiers in pediatrics",
  "versions": []
}