{
  "abstract": "Innate immune responses must be tightly controlled to maintain immuno-homeostasis. However, the regulatory mechanisms underlying the activation and early stages of the innate immune response remain poorly defined. Here, we found the soluble C-type lectin Clec18a is up-regulated in multiple inflammatory diseases, including sepsis and influenza, and secreted within minutes upon activation in multiple immune cells, including macrophages, dendritic cells (DCs), and T cells. Clec18a-myeloid-knockout mice exhibited reduced survival and exacerbated inflammation than the wild-type. However, exogenous recombinant Clec18a administration alleviated inflammation both in vitro and in vivo. Mechanistically, we identified macrophage-inducible C-type lectin (Mincle) as the receptor of Clec18a. Clec18a-Mincle binding triggers Trpm7-dependent calcium influx, which activates the ubiquitin E3 ligase Cbl and leads to Mincle-Cbl-MyD88-Trpm7 complex formation and degradation. Cbl deficiency, calcium inhibition and Trpm7 knockdown abrogated Clec18a-mediated immune suppression. Thus, our study revealed Clec18a as a critical checkpoint on the initiation of innate immune response through an intrinsic crosstalk between CLR and TLR signaling.",
  "abstract_shown": true,
  "affiliations": [
    "Changhai Hospital"
  ],
  "article_type": "New results",
  "arxiv": null,
  "author_total": 8,
  "authors": [
    {
      "name": "Z. Jiang"
    },
    {
      "name": "L. Bo"
    },
    {
      "name": "N. Li"
    },
    {
      "name": "H. Chen"
    },
    {
      "name": "T. Li"
    },
    {
      "name": "Y. Zhang"
    },
    {
      "name": "X.-m. Deng"
    },
    {
      "affs": [
        0
      ],
      "name": "J. Bian"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/cwnfr93azstj0.bib",
  "cited_by": 0,
  "doi": "10.64898/2026.09.24.754070",
  "fulltext_url": "https://www.biorxiv.org/content/10.64898/2026.09.24.754070v1.full",
  "id": "cwnfr93azstj0",
  "issns": [],
  "landing_url": "https://www.biorxiv.org/content/10.64898/2026.09.24.754070v1",
  "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",
      "2403|Immune Response and Inflammation"
    ]
  ],
  "openalex": "W7214790448",
  "pdf_url": "https://www.biorxiv.org/content/10.64898/2026.09.24.754070v1.full.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-09-24",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/cwnfr93azstj0.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:25:17Z",
      "native_id": "10.64898/2026.09.24.754070",
      "source": "biorxiv",
      "url": "https://www.biorxiv.org/content/10.64898/2026.09.24.754070v1"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "biorxiv:immunology",
      "subfield": "immunology"
    }
  ],
  "title": "Inflammation-induced of Clec18a inhibits immune responses via Trpm7-dependent Cbl activation",
  "title_text": "Inflammation-induced of Clec18a inhibits immune responses via Trpm7-dependent Cbl activation",
  "type": "preprint",
  "updated_at": "2026-10-30T12:25:17Z",
  "url": "https://research.draconitic.com/paper/cwnfr93azstj0",
  "venue": "bioRxiv",
  "versions": []
}