Cited by 46Phagocytosis and Immune RegulationInflammatory Bowel DiseaseImmune Response and Inflammation

C-type lectin receptor lsectin-mediated apoptotic cell clearance by macrophages directs intestinal repair in experimental colitis

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Yang, Zaopeng, Li, Qian, Wang, Xin, Jiang, Xuepei, Zhao, Dianyuan, Lin, Xin, He, Fuchu, Tang, Li·2018·Proceedings of the National Academy of Sciences

Abstract

Epithelial barrier disruption is a major cause of inflammatory bowel disease (IBD); however, the cellular and molecular regulation of intestinal epithelial homeostasis remains largely undefined. Here, we show that the C-type lectin receptor LSECtin (Clec4g) on macrophages is required for protection against dextran sulfate sodium-induced colitis. Mechanistically, LSECtin promotes apoptotic cell clearance by macrophages and induces the production of antiinflammatory/tissue repair factors in an engulfment-dependent manner, which in turn stimulates epithelial cell proliferation. Deletion of LSECtin results in defective engulfment by colon macrophages, leading to aberrant proresolving factor production and impaired intestinal epithelium repair. Collectively, our findings suggest that LSECtin-dependent corpse clearance by macrophages can direct intestinal regeneration and maintenance of the mucosal barrier after injury.

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Registry

Crossref · 10.1073/pnas.1804094115

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  • C-type lectin receptor LSECtin (Clec4g) on colon macrophages is required for macrophage engulfment and clearance of apoptotic cells, contributing to intestinal repair in DSS-induced colitis.

    “Yang et al. reported that the C-type lectin receptor LSECtin (Clec4g) on colon macrophages is required for macrophage engulfment and clearance of apoptotic cells, contributing to intestinal repair in dextran sulphate sodium-induced colitis [146].”

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Authors
Yang, Z., Li, Q., Wang, X., Jiang, X., Zhao, D., Lin, X., He, F., & Tang, L.
Affiliations
  • Peking University (CN)
  • Fudan University (CN)
  • Beijing Proteome Research Center (CN)
  • State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences, Beijing Institute of Lifeomics, 102206 Beijing, China;
Venue
Proceedings of the National Academy of Sciences
Published
2018-10-09
Volume
115
Issue
43
Pages
11054-11059
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2897988416
Cited by
46
References
34
Citations by year
2026: 3 · 2025: 6 · 2024: 4 · 2023: 6 · 2022: 7 · 2021: 5 · 2020: 11 · 2019: 3
FWCI
2.04
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
LSECtin, C-type lectin receptors, macrophages, efferocytosis, intestinal repair, colitis, DSS-induced colitis, inflammatory bowel disease, epithelial barrier function, epithelial cell proliferation, mucosal barrier, tissue homeostasis
MeSH terms
Animals, Colitis, Colon, Disease Models, Animal, Epithelial Cells, Intestinal Mucosa, Macrophages, Male, Mice, Inbred C57BL, Phagocytosis, Receptors, Virus, Inflammatory Bowel Diseases, Signal Transduction, Apoptosis, Lectins, C-Type, Cell Proliferation, Mice

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