ArticleArthritis research & therapy2016
JAK3-STAT pathway blocking benefits in experimental lupus nephritis.
Article in Arthritis research & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.
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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.
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Who cites it
29 citing papers in PubMed, 57 citations in OpenAlex.
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Trial
- Tubulointerstitial inflammation in glomerular diseases: mechanistic pathways, prognostic value, and translational therapeutic targets.Renal failure · 2026Review
- CD8MedComm · 2026Review
- JAK3 Staining and CD68+ Macrophage Counts Are Increased in Patients with IgA Nephropathy.Diagnostics (Basel, Switzerland) · 2026Article
- Targeting the Type I Interferon Pathway in Glomerular Kidney Disease: Rationale and Therapeutic Opportunities.Kidney international reports · 2025Review
- Therapeutic JAK1 Inhibition Reverses Lupus Nephritis in a Mouse Model and Demonstrates Transcriptional Changes Consistent With Human Disease.ACR open rheumatology · 2024Article
- Drug repurposing for glomerular diseases: an underutilized resource.Nature reviews. Nephrology · 2024Review
- JAK Inhibition as a Potential Treatment Target in Systemic Lupus Erythematosus.Mediterranean journal of rheumatology · 2024Review
- Lupus Nephritis: New and Emerging Biologic and Targeted Therapies.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2023Review
- Review
- Targeted Therapy for SLE-What Works, What Doesn't, What's Next.Journal of clinical medicine · 2023Review
- Article
- Janus kinase inhibitors in systemic lupus erythematosus: implications for tyrosine kinase 2 inhibition.Frontiers in medicine · 2023Review
- Potential Use of Janus Kinase Inhibitors in the Treatment of Systemic Lupus Erythematosus.Journal of inflammation research · 2023Review
- Utilizing a human TLR selective ligand in a humanized immune system mouse model to investigate human TLR4 signaling.Journal of biological methods · 2023Article
- Why Do We Need JAK Inhibitors in Systemic Lupus Erythematosus?International journal of molecular sciences · 2022Review
- Review
- The gene silencing of IRF5 and BLYSS effectively modulates the outcome of experimental lupus nephritis.Molecular therapy. Nucleic acids · 2021Article
- The Th17/IL-17 Axis and Kidney Diseases, With Focus on Lupus Nephritis.Frontiers in medicine · 2021Review
- Tofacitinib Ameliorates Lupus Through Suppression of T Cell Activation Mediated by TGF-Beta Type I Receptor.Frontiers in immunology · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLupus nephritis (LN) is a complex chronic autoimmune disease of unknown etiology characterized by loss of tolerance against several self-antigens. Cytokines are known to be central players in LN pathogenesis. The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway is one important pathway that mediates signal transduction of several cytokines. In this study, we examined the pathogenic role of this pathway and how CP-690,550 treatment influences LN outcome.
methodsSix-month-old NZB/NZWF1 mice were divided into two different treatment groups: (1) control animals given vehicle treatment, cyclophosphamide, and mycophenolate mofetil treatment as positive controls of the therapy and (2) mice treated with CP-690,550, a JAK3 inhibitor. Mice were treated for 12 weeks. We evaluated renal function, anti-double-stranded DNA (anti-dsDNA) antibody, renal histology changes, kidney complement and immunoglobulin G (IgG) deposits, T-cell and macrophage infiltration, kidney inflammatory gene expression, and circulating cytokine changes.
resultsCP-690,550 treatment significantly reduced proteinuria and improved renal function and histological lesions of the kidney. Compared with vehicle-treated animals, those undergoing CP-690,550 treatment showed significantly diminished anti-dsDNA antibody and complement component C3 and IgG deposition in glomeruli. We also observed a significant reduction of T-cell and macrophage infiltration. Kidney gene expression revealed a reduction in inflammatory cytokines and complement and related macrophage-attracting genes. Circulating inflammatory cytokines were also reduced with treatment.
conclusionsOn the basis of our results, we conclude that the JAK-STAT pathway is implicated in the progression of renal inflammation in NZB/WF1 mice and that targeting JAK3 with CP-690,550 is effective in slowing down the course of experimental LN. Thus, CP-690,550 could become a new therapeutic tool in LN and other autoimmune diseases.
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