ArticleeLife2025
CD131 contributes to ulcerative colitis pathogenesis by promoting macrophage infiltration.
Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Ulcerative colitis (UC) is a group of chronic inflammatory bowel disease mainly affecting the colon. The exact etiology of UC remains elusive. CD131 is a receptor subunit mediating the effects of hematopoietic growth factors granulocyte-macrophage colony-stimulating factor (GM-CSF) and Interleukin-3 (IL-3), which regulate various inflammatory responses. The pleiotropic effects of the cytokines on intestinal inflammation suggest that additional factors influence their overall function, where the receptor may play a role. Methods: In the present study, we investigated the role of CD131 in the pathogenesis of UC, with the use of murine colitis model established by administration of dextran sulfate sodium (DSS) in the drinking water. Results: By comparing the immune and inflammatory responses between wt and CD131-deficient mice, we found that CD131 contributed to DSS-induced murine colitis, which functioned in synergy with tissue-infiltrating macrophages. Besides, CD131 may have promoted the chemotaxis of macrophages and T cells into the colon through CCL4. In addition, we analyzed clinical data and pathology specimens from UC patients and found that CD131 was associated with the endoscopic and pathological severity of intestinal inflammation. Conclusions: The present study provides a novel way to the understanding of the mechanisms of GM-CSF and IL-3 effects in the intestine, which will benefit the development of therapeutic approaches. Funding: The present work has received no external funding but only from the affiliated institution.
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