C-type lectin receptor lsectin-mediated apoptotic cell clearance by macrophages directs intestinal repair in experimental colitis
Open accessAbstract
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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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].”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [146]
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Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases
Song, P., An, J., & Zou, M.-H. (2020) · Cells · doi:10.3390/cells9030671 · Cited by 198 · see citing works
“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].”
BackgroundChai, R., Ye, Z., Xue, W., Shi, S., Wei, Y., Hu, Y., & Wu, H. (2023) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2023.1252942 · Cited by 85 · see citing works
- 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
- Publisher
- National Academy of Sciences
- Published
- 2018-10-09
- Volume
- 115
- Issue
- 43
- Pages
- 11054-11059
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC6205441
- 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
- green
- www.ncbi.nlm.nih.gov
- 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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