SynthesisJournal of Crohn's & colitis2026
TL1A as a therapeutic renaissance in inflammatory bowel disease: a systematic review from molecular mechanisms to clinical translation.
Synthesis in Journal of Crohn's & colitis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Inflammatory bowel disease treatment: Mechanisms to clinical translation (Review).International journal of molecular medicine · 2026Review
- TL1A inhibitors in inflammatory bowel disease: A systematic review of phase 2 clinical trials.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsDespite major therapeutic advances, many patients with inflammatory bowel disease (IBD) continue to experience inadequate treatment response, progressive disease, and irreversible complications requiring surgery. Current management is constrained by a biological efficacy ceiling and lack of agents directly targeting key drivers of fibrosis and barrier dysfunction. This systematic review synthesizes current knowledge on tumor necrosis factor-like cytokine 1A (TL1A) and death-domain receptor 3 (DR3) signaling pathways, critically evaluates the therapeutic potential of TL1A-targeted interventions, and explores future directions for precision medicine applications in IBD care.
methodsA comprehensive systematic search of PubMed, EMBASE, Cochrane library, Web of Science, and ClinicalTrials.gov was conducted according to PRISMA guidelines. Three independent reviewers screened preclinical and clinical studies using Rayyan software. Study selection, data extraction, and quality assessment were performed in duplicate. Eligible studies underwent narrative thematic synthesis.
resultsOf 250 studies identified, 63 met inclusion criteria. Preclinical data consistently demonstrate TL1A-DR3 signaling drives inflammation, fibrosis, and barrier dysfunction. Phase 2 clinical trials showed anti-TL1A monoclonal antibodies (Tulisokibart, Afimkibart, Duvakitug) achieved clinical remission/response rates between 26% and 66% in patients with moderate-to-severe IBD at 12-14 weeks, with favorable safety profiles. Emerging themes include extended dosing intervals, therapeutic benefit in treatment-refractory populations, potential anti-fibrotic effects, and opportunities for biomarker-guided patient stratification.
conclusionTL1A inhibitors represent a promising novel therapeutic class with dual anti-inflammatory and anti-fibrotic properties, addressing critical unmet clinical needs in IBD. These agents hold the potential to become cornerstone therapies in the evolving landscape of precision medicine for IBD care.
Indexed as
Identifiers
What OpenQuestion holds
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.