ArticleFrontiers in immunology2021
Tofacitinib Suppresses Several JAK-STAT Pathways in Rheumatoid Arthritis
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 60 citations in OpenAlex.
- Differential regulation of SOCS signalling and immunoproteasome pathways by JAK inhibitors and TNF inhibitors in rheumatoid arthritis.Arthritis research & therapy · 2026Article
- Long-Term Real-World Evaluation of Tofacitinib's Effectiveness and Safety in Japan: Insights Into Optimal Timing for Dose Reduction.JGH open : an open access journal of gastroenterology and hepatology · 2026Article
- STAT Signaling in Metabolic Disorders: From Molecular Mechanisms to Therapeutic Implications.Cell biochemistry and biophysics · 2026Review
- Pro-Inflammatory Cytokines as Core Mediators of Colonic Epithelial Barrier Dysfunction: Roles of TNF-α, IFN-γ, IL-1β, and IL-6.International journal of molecular sciences · 2026Review
- JAK/STAT inhibition reprograms T cell activation and metabolism in inflammatory arthritis patients.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Targeting NF-κB and JAK/STAT pathways in rheumatoid arthritis: emerging nanocarrier-based drug delivery approaches.Inflammopharmacology · 2026Review
- Role of the STAT3 Signaling Pathway in Cell Proliferation and Inflammation in Psoriasis and Approaches for Targeted Therapies: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026Review
- Tofacitinib repairs inflammation and mitochondrial dysregulation in GM-CSF-reprogrammed RA macrophages.Cellular & molecular immunology · 2026Article
- Multiplexed high-content imaging uncovers morphological diversity of lymphocyte activation and dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Population-Based Multi-Omics and Cohort Study Identifying Predictive Biomarkers and Therapeutic Targets for Psoriatic Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mechanisms of transcriptional regulation of CCR5, which is the co-receptor for R5-tropic HIV and is also involved in other disease processes.Biochemical Society transactions · 2026Review
- Targeting CXCL8 alleviates intestinal epithelial inflammation by suppressing the JAK-STAT pathway.European journal of medical research · 2025Article
- Transcriptomic Evaluation of Hollow Microneedles-Mediated Drug Delivery for Rheumatoid Arthritis Therapy.Biosensors · 2025Article
- Reversal of partial botulinum toxin A resistance following Janus kinase inhibition with tofacitinib: A case series.JAAD case reports · 2025Article
- The genetic puzzle of rheumatoid arthritis: Causes, progression, and treatment.Biochemistry and biophysics reports · 2025Review
- Shaping Orthodontics of the Future: Concepts and Implications from a Cellular and Molecular Perspective.International journal of molecular sciences · 2025Review
- Palmoplantar Pustulosis during Pregnancy Was Successfully Treated with Tofacitinib: A Case Report.Skin appendage disorders · 2025Article
- Article
- Transcriptional Profiling of Tofacitinib Treatment in Juvenile Idiopathic Arthritis: Implications for Treatment Response Prediction.Arthritis care & research · 2025Article
- Research progress of SOCS in autoimmune diseases: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Current knowledge on the actions of tofacitinib on cytokine signaling pathways in rheumatoid arthritis (RA) is based on Methods: Sixteen patients with active RA, despite treatment with conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), received tofacitinib 5 mg twice daily for three months. Levels of constitutive and cytokine-induced phosphorylated STATs in peripheral blood monocytes, T cells and B cells were measured by flow cytometry at baseline and three-month visits. mRNA expression of JAKs, STATs and suppressors of cytokine signaling (SOCS) were measured from peripheral blood mononuclear cells (PBMCs) by quantitative PCR. Association of baseline signaling profile with treatment response was also investigated. Results: Tofacitinib, in csDMARDs background, decreased median disease activity score (DAS28) from 4.4 to 2.6 (p < 0.001). Tofacitinib treatment significantly decreased cytokine-induced phosphorylation of all JAK-STAT pathways studied. However, the magnitude of the inhibitory effect depended on the cytokine and cell type studied, varying from 10% to 73% inhibition following 3-month treatment with tofacitinib. In general, strongest inhibition by tofacitinib was observed with STAT phosphorylations induced by cytokines signaling through the common-γ-chain cytokine receptor in T cells, while lowest inhibition was demonstrated for IL-10 -induced STAT3 phosphorylation in monocytes. Constitutive STAT1, STAT3, STAT4 and STAT5 phosphorylation in monocytes and/or T cells was also downregulated by tofacitinib. Tofacitinib treatment downregulated the expression of several JAK-STAT pathway components in PBMCs, SOCSs showing the strongest downregulation. Baseline STAT phosphorylation levels in T cells and monocytes and SOCS3 expression in PBMCs correlated with treatment response. Conclusions: Tofacitinib suppresses multiple JAK-STAT pathways in cytokine and cell population specific manner in RA patients
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