{
  "abstract": "Clearance of dead cells by efferocytosis is a critical process for homeostasis, notably by limiting inflammation. Defective efferocytosis has been associated with autoimmune, neurodegenerative, and cardiovascular diseases, as well as chronic infections, making its regulation a potential therapeutic target. Here, we identify circulating cochlin LCCL (Limulus factor C, Cochlin, and Lgl1) domain as a regulator of efferocytosis. Using cell binding assay for recombinant cochlin LCCL domain, we establish its tropism for dead or dying cells of both immune and non-immune lineages from murine and human origins. By three independent functional assays, we demonstrate that endogenous and exogenous cochlin LCCL domain enhances macrophage efferocytosis in vitro and in vivo in lipopolysaccharide (LPS)-induced inflammation and intranasal Pseudomonas aeruginosa infection, to a similar extent as the efferocytosis promoter GAS6. Our findings provide a role of cochlin LCCL domain in the regulation of efferocytosis, alongside its already described pro-inflammatory role, as an immunomodulator for host response and homeostasis.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": null,
  "arxiv": null,
  "author_total": 12,
  "authors": [
    {
      "name": "Louise Courcol"
    },
    {
      "name": "Ali Hassan"
    },
    {
      "name": "Zofia Haftek-Terreau"
    },
    {
      "name": "Clara Vigneron"
    },
    {
      "name": "Ananga Ghosh"
    },
    {
      "name": "Lucie Collombet"
    },
    {
      "name": "Stefan Tholen"
    },
    {
      "name": "Gaëtan Juban"
    },
    {
      "name": "Anne-Claire Lukaszewicz"
    },
    {
      "name": "Oliver Schilling"
    },
    {
      "name": "Bénédicte F Py"
    },
    {
      "name": "Fabienne Venet"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/en1hpbsayf42y.bib",
  "cited_by": 0,
  "doi": "10.1016/j.celrep.2026.117771",
  "fulltext_url": null,
  "id": "en1hpbsayf42y",
  "issns": [
    "2211-1247",
    "2211-1247"
  ],
  "landing_url": "https://hal.science/hal-05775966v1",
  "language": "en",
  "licence": "CC-BY-NC-4.0",
  "licence_label": "CC BY-NC 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by-nc/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "hal",
      "0.sdv"
    ],
    [
      "hal",
      "1.sdv.bc"
    ],
    [
      "hal",
      "1.sdv.mhep"
    ],
    [
      "hal",
      "2.sdv.bc.ic"
    ],
    [
      "openalex",
      "2403|Phagocytosis and Immune Regulation"
    ]
  ],
  "openalex": "W7172396427",
  "pdf_url": "https://hal.science/hal-05775966/document",
  "pmcid": null,
  "pmid": "42555352",
  "published": "2026-10-02",
  "publisher": "Elsevier Inc",
  "ris": "https://research.draconitic.com/paper/en1hpbsayf42y.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:17:46Z",
      "native_id": "hal-05775966",
      "source": "hal",
      "url": "https://hal.science/hal-05775966v1"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "hal:1.sdv.bc",
      "subfield": "cell-biology"
    },
    {
      "field": "medicine",
      "origin": "hal:1.sdv.mhep",
      "subfield": "general"
    }
  ],
  "title": "Circulating cochlin LCCL domain binds to dying cells and enhances efferocytosis",
  "title_text": "Circulating cochlin LCCL domain binds to dying cells and enhances efferocytosis",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:17:46Z",
  "url": "https://research.draconitic.com/paper/en1hpbsayf42y",
  "venue": "Cell Reports",
  "versions": []
}