ArticleJournal of translational medicine2026
IL1β
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Review
- Multimodal biomarkers and prediction models for stricturing and penetrating progression in Crohn's disease.Frontiers in medicine · 2026Review
- Macrophage dysregulation in inflammatory bowel disease: cellular heterogeneity, pathogenic mechanism, and treatment.Frontiers in immunology · 2026Review
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Authors and funding
20 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExcessive extracellular matrix deposition is a hallmark of intestinal fibrosis in Crohn’s disease (CD), with fibroblasts playing a central pathogenic role. This study aimed to elucidate how macrophages regulate fibroblast activity and contribute to intestinal fibrosis development in CD.
methodsSingle-cell RNA sequencing (scRNA-seq) data from the Cleveland and MGH cohorts were integrated to identify IL1β+ macrophages and PI16+ fibroblasts involved in CD-associated fibrosis. Subsequently, above cell–cell interactions were validated by in vitro experiments such as flow cytometry, co-culture assays, ELISA and western blotting. The functional role of amphiregulin (AREG) and its neutralizing antibody AR37 was further assessed in the DSS-induced chronic intestinal fibrosis mice models.
resultsPI16+ fibroblasts exhibited the highest ECM score, indicating their prominent role in extracellular matrix production. IL1β+ macrophages showed the highest pro-fibrotic signature score, suggesting strong pro-fibrotic potential. The ligand–receptor analysis revealed AREG–EGFR interactions between IL1β+ macrophages and PI16+ fibroblasts. The scRNA-seq data identified IL1β+ macrophages as the predominant cellular source of pro-fibrotic factor AREG. Moreover, the in-vitro assays revealed that IL1β+ macrophages promoted proliferation and activation of PI16+ fibroblasts by secreting AREG. The animal experiment results revealed that AREG neutralizing antibody AR37 attenuated PI16 + fibroblasts expansion and intestinal fibrosis in DSS-induced chronic fibrosis models.
conclusionIL1β+ macrophages promote intestinal fibrosis of CD by increasing proliferation and activation of PI16 + fibroblasts via AREG-EGFR signaling. Targeting the AREG-EGFR signaling could disrupt IL1β+ macrophages-PI16+ fibroblasts crosstalk to mitigate intestinal fibrosis progression in CD.
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