ReviewGut2025
Targeting TL1A and DR3: the new frontier of anti-cytokine therapy in IBD.
Review in Gut, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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
26 citing papers in PubMed, 1 synthesis or guideline pooled it.
- TL1A as a therapeutic renaissance in inflammatory bowel disease: a systematic review from molecular mechanisms to clinical translation.Journal of Crohn's & colitis · 2026Pooled it
- Article
- Integrating Patient-Centric Clinical Pharmacology and MID3 to Advance Biologic Development in Immune-Mediated Inflammatory Diseases.Clinical pharmacology and therapeutics · 2026Review
- Targeted Therapies in Inflammatory Bowel Disease: Mechanisms, Comparative Evidence, and Clinical Translation.Journal of clinical medicine · 2026Review
- Inflammatory and Immune Cytoprofiles of Active Ulcerative Colitis from Crohn's Disease-Insights from Multivariable Modeling.International journal of molecular sciences · 2026Article
- Recent advances in the management of small bowel Crohn's disease.The Korean journal of internal medicine · 2026Review
- TL1A/DR3 signaling deletion attenuates mucosal inflammation and alveolar bone loss in a murine model of spontaneous periodontitis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Elevated caspase 3 expression correlates with severe inflammation in Crohn's disease.European journal of histochemistry : EJH · 2026Article
- The RNA methyltransferase NSUN2 catalyzes 5-methylcytosine (mThe Journal of biological chemistry · 2026Article
- Therapeutic Potential of Tulisokibart and Anti-TL1A Therapy in Inflammatory Disorders: Current Insights and Future Directions.Clinical reviews in allergy & immunology · 2026Review
- Activation of the Nrf2 Signaling Pathway by a Ginseng-Salvia Root-Notoginseng Composite Alleviates Ulcerative DSS-Induced Colitis via Restoring Gut Microbiota and the Intestinal Barrier.Antioxidants (Basel, Switzerland) · 2026Article
- Article
- Article
- Microbial mechanisms and therapeutic interventions in the periodontitis-inflammatory bowel disease axis: a comprehensive review.Journal of oral microbiology · 2026Review
- Advancing therapeutic frontiers: a pipeline of novel drugs for UC management.Frontiers in gastroenterology (Lausanne, Switzerland) · 2026Review
- The Therapeutic Potential of Targeting TL1A in a Spectrum of Inflammatory Disorders.Journal of inflammation research · 2026Review
- Engineering Nanomaterial Platform for Inflammatory Bowel Disease: Three-Dimensional Integration of Delivery Mechanism, Therapeutic Drug Delivery and Intelligent Material Design.International journal of nanomedicine · 2026Review
- Selective Nanoparticulate Systems for Drug Delivery in Inflammatory Bowel Disease.Pharmaceutics · 2025Review
- Dynamic neutrophil-keratinocyte communication network centered on IL-36/TNFSF15 responses characterizes inflammatory responses in generalized pustular psoriasis.Nature communications · 2025Article
- Gene-environment interactions shape the host-microbial interface in inflammatory bowel disease.Nature immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
TNF-like cytokine 1A (TL1A) and its functional receptor, death-domain receptor 3 (DR3), are members of the TNF and TNFR superfamilies, respectively, with recognised roles in regulating innate and adaptive immune responses; additional existence of a decoy receptor, DcR3, indicates a tightly regulated cytokine system. The significance of TL1A:DR3 signalling in the pathogenesis of inflammatory bowel disease (IBD) is supported by several converging lines of evidence. Herein, we aim to provide a comprehensive understanding of what is currently known regarding the TL1A/DR3 system in the context of IBD. TL1A and DR3 are expressed by cellular subsets with important roles for the initiation and maintenance of intestinal inflammation, serving as potent universal costimulators of effector immune responses, indicating their participation in the pathogenesis of IBD. Recent evidence also supports a homoeostatic role for TL1A:DR3 via regulation of Tregs and innate lymphoid cells. TL1A and DR3 are also expressed by stromal cells and may contribute to inflammation-induced or inflammation-independent intestinal fibrogenesis. Finally, discovery of genetic polymorphisms with functional consequences may allow for patient stratification, including differential responses to TL1A-targeted therapeutics. In conclusion, TL1A:DR3 signalling plays a central and multifaceted role in the immunological pathways that underlie intestinal inflammation, such as that observed in IBD. Such evidence provides the foundation for developing pharmaceutical approaches targeting this ligand-receptor pair in IBD.
Indexed as
Identifiers
What Socratic 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 Socratic graph.