ArticleGut2026
TL1A-activated T cells remodel the rectal mucosa in patients with Crohn's disease with perianal fistulising disease.
Article in Gut, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- BRD4 contributes to the cytokine-induced acquisition of an IL-13RA2-positive inflammatory fibroblast phenotype.Journal of Crohn's & colitis · 2026Article
- Crohn's Disease: From Immune Dysregulation to Intestinal Damage.Inflammation · 2026Review
- Impaired keratinization activity in perianal Crohn's fistulas is associated with poor prognosis.Journal of Crohn's & colitis · 2026Article
- Multiomics analysis dissects the molecular foundation of perianal fistulas associated with Crohn's disease and of cryptoglandular origin.Journal of Crohn's & colitis · 2026Article
- Multimodal biomarkers and prediction models for stricturing and penetrating progression in Crohn's disease.Frontiers in medicine · 2026Review
Corrections and comments
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Authors and funding
27 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPerianal fistulising disease (PFD) is a complication that affects about 20% of patients with Crohn's disease (CD) whose aetiology remains unknown.
objectivesTo identify predisposing events driving fistula formation.
designRectal biopsies from patients with CD with or without PFD (CD+PFD and CD, respectively; n=31) were collected and subjected to single-cell RNA sequencing. Functional analyses were conducted using peripheral CD3
resultsThe rectal mucosa of patients with CD+PFD is imprinted with cellular and transcriptomic alterations specific to PFD and independent of luminal inflammation, potentially driven by tumour necrosis factor-like ligand 1A (TL1A) activation in CD4
conclusionOur findings revealed unique cellular alterations in the rectum of patients with CD+PFD, highlighting the previously unrecognised involvement of TL1A in mediating this signature and supporting the need for exploring the role of TL1A inhibition as a therapeutic approach for PFD.
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