ArticleGut2019
Expansion of IL-23 receptor bearing TNFR2+ T cells is associated with molecular resistance to anti-TNF therapy in Crohn's disease.
Article in Gut, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03802214 (A Case-control Study to Evaluate the Immunoinflammatory Effect of Prior Exposure to Anti-TNF Therapy in Patients With Ulcerative Colitis Starting Vedolizumab Therapy), which is not on this map. Cited by 149 papers, 9 of them syntheses that pooled it.
What it found
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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.
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.
A Case-control Study to Evaluate the Immunoinflammatory Effect of Prior Exposure to Anti-TNF Therapy in Patients With Ulcerative Colitis Starting Vedolizumab Therapy
Who cites it
149 citing papers in PubMed, 9 syntheses or guidelines pooled it, 246 citations in OpenAlex.
- Efficacy and Safety of Risankizumab in Crohn's Disease: A Systematic Review and Meta-Analysis of Randomized Trials and Real-World Evidence.Digestive diseases and sciences · 2026Pooled it
- Systematic Review With Meta-Analysis: Safety and Effectiveness of Combining Biologics and Small Molecules in Inflammatory Bowel Diseases.Inflammatory bowel diseases · 2026Pooled it
- The predictive value of machine learning for the response to anti-TNF-α therapy in patients with Crohn's disease: a systematic review and meta-analysis.Frontiers in immunology · 2026Pooled it
- Comparative Efficacy of Advanced Therapies for Management of Moderate-to-Severe Crohn's Disease: 2025 AGA Evidence Synthesis.Gastroenterology · 2025Pooled it
- IL-23p19 Antagonists vs Ustekinumab for Treatment of Crohn's Disease: A Meta-Analysis of Randomized Controlled Trials.The American journal of gastroenterology · 2025Pooled it
- Systematic review and bayesian network meta-analysis: comparative efficacy and safety of six commonly used biologic therapies for moderate-to-severe Crohn's disease.Frontiers in pharmacology · 2024Pooled it
- Efficacy and Safety of IL-12/23 and IL-23 Inhibitors for Crohn's Disease: Systematic Review and Meta-Analysis.Digestive diseases and sciences · 2023Pooled it
- Comparative efficacy and safety of biologic therapies for moderate-to-severe Crohn's disease: a systematic review and network meta-analysis.The lancet. Gastroenterology & hepatology · 2021Pooled it
- Pooled it
- A fasting-mimicking diet in patients with mild-to-moderate Crohn's disease: a randomized controlled trial.Nature medicine · 2026Trial
- Randomized Controlled Trial Substudy of Cell-specific Mechanisms of Janus Kinase 1 Inhibition With Upadacitinib in the Crohn's Disease Intestinal Mucosa: Analysis From the CELEST Study.Inflammatory bowel diseases · 2021Trial
- Uninflamed colonic tissue harbors humoral activity linked to anti-TNF therapy non-response in ulcerative colitis.iScience · 2026Article
- A case of refractory immune checkpoint inhibitor-induced colitis successfully treated with mirikizumab.Clinical journal of gastroenterology · 2026Article
- Comparative Effectiveness of Biologic Therapies in Chronic Pouchitis and Crohn's-Like Disease of the Pouch: A Bi-center Retrospective Cohort Study.Digestive diseases and sciences · 2026Article
- Comparing the Efficacy of Advanced Interleukin Inhibitors for Crohn's Disease: A Systematic Review and Network Meta-Analysis.Journal of clinical medicine · 2026Review
- Patients with Crohn's Disease Achieving Ustekinumab-Induced Remission Are Characterized by Increased Baseline IL-23 Receptor Expression on Lamina Propria Th1 Cells.Journal of clinical medicine · 2026Article
- Role of PANoptosis in intestinal diseases and its therapeutic implications.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Tissue transcriptional programs stratify Crohn's disease by therapeutic response and clinical outcomes.Scientific reports · 2026Article
- Efficacy and safety of dual biologics or combination therapy with JAK inhibitors in refractory inflammatory bowel disease: a retrospective single-center real-world study from China.BMC gastroenterology · 2026Article
- Interleukin-23 Inhibitors in Inflammatory Bowel Disease.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
89 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveAnti-tumour necrosis factor (TNF) antibodies are successfully used for treatment of Crohn's disease. Nevertheless, approximately 40% of patients display failure to anti-TNF therapy. Here, we characterised molecular mechanisms that are associated with endoscopic resistance to anti-TNF therapy.
designMucosal and blood cells were isolated from patients with Crohn's disease prior and during anti-TNF therapy. Cytokine profiles, cell surface markers, signalling proteins and cell apoptosis were assessed by microarray, immunohistochemistry, qPCR, ELISA, whole organ cultures and FACS.
resultsResponders to anti-TNF therapy displayed a significantly higher expression of TNF receptor 2 (TNFR2) but not IL23R on T cells than non-responders prior to anti-TNF therapy. During anti-TNF therapy, there was a significant upregulation of mucosal IL-23p19, IL23R and IL-17A in anti-TNF non-responders but not in responders. Apoptosis-resistant TNFR2+IL23R+ T cells were significantly expanded in anti-TNF non-responders compared with responders, expressed the gut tropic integrins α4β7, and exhibited increased expression of IFN-γ, T-bet, IL-17A and RORγt compared with TNFR2+IL23R- cells, indicating a mixed Th1/Th17-like phenotype. Intestinal TNFR2+IL23R+ T cells were activated by IL-23 derived from CD14+ macrophages, which were significantly more present in non-responders prior to anti-TNF treatment. Administration of IL-23 to anti-TNF-treated mucosal organ cultures led to the expansion of CD4+IL23R+TNFR2+ lymphocytes. Functional studies demonstrated that anti-TNF-induced apoptosis in mucosal T cells is abrogated by IL-23.
conclusionsExpansion of apoptosis-resistant intestinal TNFR2+IL23R+ T cells is associated with resistance to anti-TNF therapy in Crohn's disease. These findings identify IL-23 as a suitable molecular target in patients with Crohn's disease refractory to anti-TNF therapy.
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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.