ReviewFrontiers in immunology2025
The role of the tuft cell-interleukin-25 axis in the pathogenesis of inflammatory bowel disease.
Review in Frontiers in immunology, 2025. 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.
- Lactobacilli Mitigate Gut Inflammation by Modulating T-Helper/T-Regulatory Cells and Suppressing Signaling Pathways in Food-Derived Models.Probiotics and antimicrobial proteins · 2026Review
- Roles for specialized secretory epithelial cells in inflammatory bowel disease.Current opinion in gastroenterology · 2026Review
- New-onset allergic diseases after SARS-CoV-2 infection: mechanistic hypotheses and emerging strategies for risk stratification.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence highlights the tuft cell-Interleukin-25 (IL-25) axis (tuft/IL-25 axis) as a critical orchestrator bridging luminal stimuli and intestinal immunity in Inflammatory Bowel Disease (IBD), which encompasses Crohn's Disease (CD) and Ulcerative Colitis (UC). This review synergises current understanding of how dysregulation within this axis contributes to IBD pathogenesis, arising from disrupted immune homeostasis involving aberrant microbiota responses, genetic susceptibility, and immune pathway dysregulation. Central to this axis, intestinal tuft cells act as chemosensory epithelial sentinels, differentiating in response to microbial and metabolic cues to become the primary source of IL-25. IL-25, signaling via IL-17RB, engages innate and adaptive immune cells, particularly group 2 innate lymphoid cells (ILC2s). While IL-33-responsive homeostatic ILC2s (nILC2s) promote mucosal repair, IL-25-driven inflammatory ILC2s (iILC2s) amplify inflammation, positioning them as pivotal effectors. Critically, IL-25 exhibits a context-dependent "double-edged" role: engagement with IL-25R
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.