Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 115, Issue 43, Pages 11054-11059Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1804094115
Keywords
macrophage; C-type lectin receptor; apoptotic cell clearance; intestinal regeneration
Categories
Funding
- Chinese National Natural Science Foundation Project [81500428]
- Beijing Natural Science Foundation Project [7182035]
- Chinese State Key Program in Basic Research [2013CB910802, 2014CBA02000]
- National Key R&D Program of China [2018YFA0507500]
- Beijing Science Program for the Top Young [2015000021223TD04]
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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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