ArticleJournal of Crohn's & colitis2024
Histological Outcomes and JAK-STAT Signalling in Ulcerative Colitis Patients Treated with Tofacitinib.
Article in Journal of Crohn's & colitis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Endo-histologic outcomes in patients with ulcerative colitis responding to tofacitinib.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2026Observational
- A metabolic constraint in de novo NAD+ synthesis drives mucosal inflammation in IBD.Journal of Crohn's & colitis · 2026Article
- Intestinal epithelial cell-specific deletion of Jak2 disrupts gut homeostasis.Scientific reports · 2026Article
- NLRP12 Deficiency Enhances Tofacitinib Efficacy in DSS Colitis Via STAT1-M1 Polarization.Inflammation · 2026Article
- Elucidating the Action Mechanism of Shenling Baizhu Powder in the Treatment of Ulcerative Colitis Based on Network Pharmacology and Experimental Validation.Combinatorial chemistry & high throughput screening · 2026Article
- Gut microbiota-derived metabolites and IL-22 signaling in inflammatory bowel disease: context-dependent regulation of mucosal repair and inflammation.Frontiers in immunology · 2026Review
- Mucosal kinase activity and inflammatory profiles in inflammatory bowel disease, and in relation to tofacitinib response.Journal of Crohn's & colitis · 2025Article
- Pioglitazone mitigates acetic acid-induced colitis in rats via epigenetic-modulation and antioxidant mechanisms.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Development of Glycyrrhizic Acid Nanoparticles for Modulating Gastric Ulcer Healing: A Comparative In Vivo Study Targeting Oxidative Stress and Inflammatory Pathways.Antioxidants (Basel, Switzerland) · 2025Article
- Exploring the Regulatory Mechanism of Total Alkaloids fromInternational journal of molecular sciences · 2025Article
- The Cell-Specific Effects of JAK1 Inhibitors in Ulcerative Colitis.Journal of clinical medicine · 2025Review
- Oral colon-targeted responsive chitosan/pectin-based nanoparticles propels the application of tofacitinib in colitis therapy.Scientific reports · 2025Article
- Multiomics Integration and Machine Learning Reveal Colony Stimulating Factor 3 Receptor as a Key Gene and Therapeutic Target in Crohn's Disease.Mediators of inflammation · 2025Article
- Exploring shared pathogenic mechanisms and biomarkers in hepatic fibrosis and inflammatory bowel disease through bioinformatics and machine learning.Frontiers in immunology · 2025Article
- Natural products for the treatment of ulcerative colitis: focus on the JAK/STAT pathway.Frontiers in immunology · 2025Review
- Bile acid metabolism modulates intestinal immunity involved in ulcerative colitis progression.Heliyon · 2024Article
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Authors and funding
13 authors.
Funding
Abstract
BACKGROUND AND
aimsHistological outcomes and JAK-STAT signalling were assessed in a prospective ulcerative colitis [UC] patient cohort after 8 weeks treatment with tofacitinib, an oral Janus kinase [JAK] inhibitor.
methodsForty UC patients received tofacitinib 10 mg twice daily for 8 weeks. Treatment response was defined as histo-endoscopic mucosal improvement [HEMI]. Histological remission was defined as a Robarts Histopathology Index [RHI] ≤3 points and histological response as 50% decrease in RHI. Mucosal expression of JAK1-3, tyrosine kinase 2 [TYK2], and total signal transducer and activator of transcription [STAT] 1-6 were assessed using immunohistochemistry [IHC].
resultsAt baseline, the median RHI was 14 (interquartile range [IQR] 10-19). Of 40 [65%] patients, 26 had severe endoscopic disease [endoscopic Mayo score 3] and 31/40 [78%] failed prior anti-tumour necrosis factor [anti-TNF] treatment. At Week 8, 15 patients [38%] had HEMI, 23 patients [58%] histological remission, and 34 [85%] histological response. RHI decreased by a median of 14 points [IQR 9-21] in responders [p <0.001] and by 6 points [IQR 0-13] in non-responders [p = 0.002]. STAT1, STAT3, and STAT5 expression levels decreased significantly in the whole cohort. Responders had lower Week 8 STAT1 expression levels compared with non-responders [0.2%, IQR 0.1-2.8 vs 4.3%, IQR 1.2-11.9, p = 0.001], suggesting more profound STAT1 blockade. A trend of higher baseline JAK2 expression was observed in tofacitinib non-responders [2.7%, IQR 0.1-7.7] compared with responders [0.4%, IQR 0.1-2.1].
conclusionsTofacitinib treatment resulted in histological improvement in the majority of UC patients and in a substantial decrease of STAT1, STAT3, and STAT5 expression. HEMI was associated with more profound suppression of STAT1.
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