ArticleBlood2025
Ruxolitinib targets JAK-STAT signaling to modulate neutrophil activation in refractory macrophage activation syndrome.
Article in Blood, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- HLHRUXO: a prospective trial of a ruxolitinib-containing regimen for children with hemophagocytic lymphohistiocytosis.Blood advances · 2026Trial
- Ruxolitinib and decitabine plus a busulfan-cyclophosphamide conditioning regimen for relapse prophylaxis in patients with high-risk acute myeloid leukemia or myelodysplastic syndromes.Frontiers in immunology · 2025Trial
- A Rare RIPK3 Variant Enhances Necroptosis and Promotes Inflammation in a Still Disease-Like Autoinflammatory Syndrome.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- The value of C-X-C motif chemokine ligand 9 (CXCL9) in the differential diagnosis and management of haemophagocytic lymphohistiocytosis.British journal of haematology · 2026Article
- Autoantibodies and T Cells Target Citrullinated and Homocitrullinated Antigens in Rheumatoid Arthritis.Immunological reviews · 2026Review
- [Mechanism and clinical progress of JAK inhibitors in hemophagocytic lymphohistiocytosis].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Review
- Amelioration of acute liver failure by a cinnamic acid derivative through inhibition of the ROS-NETosis axis.Molecular biomedicine · 2026Article
- Still's Disease and Autoinflammation: Positioning an Inflammatory Syndrome on the Autoinflammation-Autoimmunity Spectrum.Current rheumatology reports · 2026Review
- Network Pharmacology-Serum Metabolomics Integration Identifies Key Targets, Biomarkers and Mechanism of Sendeng-4 in Rheumatoid Arthritis Therapy.International journal of general medicine · 2026Article
- Case Report: Hemophagocytic lymphohistiocytosis masquerading as drug-induced liver injury: successful treatment with low-dose ruxolitinib and glucocorticoids.Frontiers in immunology · 2026Article
- Ruxolitinib combined with corticosteroids for the successful treatment of kawasaki disease-associated macrophage activation syndrome: a case report.Frontiers in pediatrics · 2026Article
- Ruxolitinib for rheumatic disease-associated macrophage activation syndrome in children: a retrospective cohort study.Frontiers in immunology · 2026Article
- Ruxolitinib reverses systemic vasculitis driven by JAK2 V617F-mutated essential thrombocythemia: a case report.Frontiers in immunology · 2026Article
- Low-dose emapalumab treatment in refractory macrophage activation syndrome secondary to adult onset still's disease/systemic lupus erythematosus: insights from nine cases.Frontiers in immunology · 2025Article
- Expression and clinical significance of S100A8/9 in adults with secondary phagocytic lymphohistiocytosis.Frontiers in molecular biosciences · 2025Article
- Efficacy and safety of ruxolitinib in adult patients with refractory rheumatic disease-associated macrophage activation syndrome.Frontiers in immunology · 2025Article
- Bioinformatics based exploration of the anti-liver fibrosis mechanism of Pien Tze Huang via EGFR/JAK1/STAT3 pathway.Frontiers in immunology · 2025Article
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Authors and funding
21 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractMacrophage activation syndrome (MAS) is believed to be caused by inappropriate proliferation and activation of the mononuclear phagocytic system. Adult-onset Still disease (AOSD) is characterized by neutrophil activation and a cytokine storm, which can lead to the severe and potentially life-threatening complication of MAS. RNA sequencing revealed that neutrophils may play a distinct role and enhance the innate immunity of patients with AOSD with MAS (AOSD-MAS). In the CpG-induced secondary hemophagocytic lymphohistiocytosis (HLH) model, the depletion of neutrophils significantly reduced cytokine levels with effects comparable with monocyte depletion. Significant enrichment was observed in the type I/II interferon and JAK-STAT pathways in neutrophils from patients with AOSD-MAS. Treatment of 10 patients with refractory AOSD-MAS with ruxolitinib led to the resolution of inflammatory parameters and clinical symptoms. RNA sequencing and ex vivo assays confirmed that ruxolitinib suppressed aberrant NETosis and STAT3/STAT5 signaling. In vivo, PAD4 knockout further confirmed the pathogenic role of NETosis in a secondary HLH model. Moreover, the selective inhibition of STAT3 or STAT5 alleviated systemic inflammation. Ten functional variants were identified in genes related to the JAK-STAT pathway, however, their clinical relevance requires further validation. These findings suggest that ruxolitinib has the potential to facilitate disease remission in patients with refractory AOSD-MAS by broadly inhibiting JAK-STAT signaling and modulating neutrophil activation and NETosis.
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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 Socratic graph.