ArticleBMC research notes2021
Interferon-γ induces interleukin-6 production by neutrophils via the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway.
Article in BMC research notes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Joint inference of paired dynamical gene regulatory networks reveals distinct cell-state landscapes of neutrophil reprogramming.bioRxiv : the preprint server for biology · 2026Article
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- Genome-wide association study reveals loci associated with cytokine levels in chicken serum.Poultry science · 2026Article
- Advancements in myelofibrosis management: a comprehensive analysis of Ojjaara (Momelotinib) therapy and clinical perspectives.Annals of medicine and surgery (2012) · 2025Review
- Upadacitinib in a Refractory Case of Alpha-1 Antitrypsin Deficiency-Related Panniculitis.Cureus · 2025Article
- Article
- Higher levels of VEGF-A and TNFα in patients with immune checkpoint inhibitor-induced inflammatory arthritis.Arthritis research & therapy · 2025Article
- P2RX1 in neutrophils mediates JAK/STAT signaling pathway to regulate malignant phenotype of gastric Cancer cells.Molecular genetics and genomics : MGG · 2025Article
- The Micro-Immunotherapy Medicine 2LPAPICancers · 2024Article
- JAK-STAT signaling in inflammation and stress-related diseases: implications for therapeutic interventions.Molecular biomedicine · 2023Review
- Inflammatory hypotheses of sleep disturbance - depression link: Update and research agenda.Brain, behavior, & immunity - health · 2023Article
- Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
objectiveInterferon-gamma (IFN-γ) is overexpressed in rheumatoid synovium and thought to be involved in the pathogenesis of rheumatoid arthritis (RA). In this study, we examined our hypothesis that IFN-γ activates innate immune cells and upregulates inflammatory cytokines. Peripheral blood neutrophils were stimulated with IFN-γ in the presence or absence of Janus kinase (JAK) inhibitors. Interleukin-6 (IL-6) mRNA and protein expression were analyzed using real-time polymerase chain reaction (PCR) method and enzyme-linked immunosorbent assay. Protein phosphorylation of JAKs or STAT1 was assessed by Western blot using phospho-specific antibodies.
resultsIFN-γ stimulation induces IL-6 expression in protein and mRNA levels in human neutrophils. Furthermore, IFN-γ stimulation induces JAK1/JAK2 phosphorylation and downstream signal transducer and activator of transcription (STAT) 1 phosphorylation in human neutrophils. Although all JAKi, blocked IFN-γ-induced JAK1.2/STAT1 phosphorylation at higher concentrations (100 nM), baricitinib most efficiently inhibited IFN-γ-induced JAK1.2/STAT1 phosphorylation at lower concentrations (≤ 25 nM). Among these JAKi, baricitinib was the most potent regulator for IFN-γ-induced IL-6 production in human neutrophils. Our data indicate that IFN-γ upregulates IL-6 production via the JAK1/2-STAT1 pathway in human innate immune cells. Furthermore, this IFN-γ-mediated IL-6 induction via JAK/STAT was downregulated by JAKi.
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