{
  "abstract": "Pathological angiogenesis is a hallmark of cancer and other chronic diseases, yet therapeutic strategies remain largely focused on blocking pro-angiogenic signals rather than restoring endogenous mechanisms that restrain endothelial sprouting. The identification of endothelial checkpoints capable of limiting pathological vessel growth therefore remains an important unmet need. CD160 is a glycosylphosphatidylinositol-anchored immunoglobulin-superfamily receptor of cytotoxic lymphocytes and an inhibitory checkpoint receptor on CD4 T cells. It is also present on endothelium and has been targeted therapeutically. Here, we identify CD160 as an inducible endothelial checkpoint that emerges in response to pro-angiogenic cues and limits pathological angiogenesis. CD160 is absent in resting endothelium. It is induced by basic fibroblast growth factor (bFGF) and most strongly by combining VEGF-A and bFGF, and it is detected in the sprouting region of ex vivo mouse aortic rings. Targeting of CD160 using monoclonal antibody reduces tubulogenesis, scratch closure and aortic-ring sprouting, and softens the cell cortex, while viability and membrane integrity remain intact. Mechanistically, CD160 associates with the endocytic receptor LRP1 as demonstrated by proximity ligation assay, lipid-raft co-immunoprecipitation and super-resolution fluorescence microscopy. Both receptors appear in a common complex, and two independent computational methods converge on the first ligand-binding cluster of LRP1 as the interface. Silencing CD160 or LRP1 abolishes the anti-angiogenic response mediated by the antibody. Under a chloroquine clamp, engagement raises autophagic flux in a CD160- and LRP1-dependent manner, and lysosomal or LDL-receptor-family blockade removes the anti-sprouting effect. CD160 therefore acts as an inducible endothelial checkpoint that suppresses sprouting through autophagic flux. Thus, CD160 represents an inducible endothelial checkpoint that is activated in a pro-angiogenic environment, and targeting CD160 restrains pathological angiogensis.",
  "abstract_shown": true,
  "affiliations": [
    "Universite de Reims Champagne-Ardenne, UMR CNRS/URCA 7369 MEDyC, Reims, France"
  ],
  "article_type": "New results",
  "arxiv": null,
  "author_total": 13,
  "authors": [
    {
      "name": "A.-I. Aziz"
    },
    {
      "name": "M. Mocquery-Corre"
    },
    {
      "name": "A. Berquand"
    },
    {
      "name": "J. Thevenard-Devy"
    },
    {
      "name": "A. Martins"
    },
    {
      "name": "C. Hachet"
    },
    {
      "name": "S. Potteaux"
    },
    {
      "name": "Y. Merrouche"
    },
    {
      "name": "R. El Fatimy"
    },
    {
      "name": "L. Duca"
    },
    {
      "name": "A. Bensussan"
    },
    {
      "name": "S. Ben Mkaddem"
    },
    {
      "affs": [
        0
      ],
      "name": "J. Devy"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/8r37s5g4rstxc.bib",
  "cited_by": 0,
  "doi": "10.64898/2026.10.19.760050",
  "fulltext_url": "https://www.biorxiv.org/content/10.64898/2026.10.19.760050v1.full",
  "id": "8r37s5g4rstxc",
  "issns": [],
  "landing_url": "https://www.biorxiv.org/content/10.64898/2026.10.19.760050v1",
  "language": null,
  "licence": "CC-BY-ND",
  "licence_label": "CC BY-ND",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by-nd/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "biorxiv",
      "immunology"
    ],
    [
      "openalex",
      "1312|Angiogenesis and VEGF in Cancer"
    ]
  ],
  "openalex": "W7223276069",
  "pdf_url": "https://www.biorxiv.org/content/10.64898/2026.10.19.760050v1.full.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-10-19",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/8r37s5g4rstxc.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:29:21Z",
      "native_id": "10.64898/2026.10.19.760050",
      "source": "biorxiv",
      "url": "https://www.biorxiv.org/content/10.64898/2026.10.19.760050v1"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "biorxiv:immunology",
      "subfield": "immunology"
    }
  ],
  "title": "CD160 is an inducible endothelial checkpoint that suppresses sprouting angiogenesis through LRP1-dependent autophagy",
  "title_text": "CD160 is an inducible endothelial checkpoint that suppresses sprouting angiogenesis through LRP1-dependent autophagy",
  "type": "preprint",
  "updated_at": "2026-10-30T12:29:21Z",
  "url": "https://research.draconitic.com/paper/8r37s5g4rstxc",
  "venue": "bioRxiv",
  "versions": []
}