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Type I and II interferons drive inflammation through STAT1 in murine macrophage activation syndrome.

GSE287998 Mus musculus Expression profiling by high throughput sequencing; Other 8 samples Submitted 2026/01/28 Platform GPL24247
Summary
Macrophage activation syndrome (MAS) exemplifies a cytokine storm syndrome by liver inflammation whereby interferon (IFN)-γ, which activates the JAK1/2-STAT1 pathway, is being a key driver cytokine. Ruxolitinib, a JAK1/2 inhibitor, has shown promising results in treating MAS patients, however the exact mechanism responsible for disease remission is unclear. One of the mediators inhibited by Ruxolitinib is STAT1, but its role in MAS pathogenesis remains unexplored. In this study, we explored the hepatic immune landscape of MAS and the role of STAT1 herein, using a Toll-like receptor (TLR)9-induced murine model of MAS. Cellular indexing of transcriptomes and epitopes-single cell RNA sequencing (CITE-seq) was performed on the immune compartment of the livers from wild-type (WT) and STAT1 knockout (KO) mice in naive conditions and upon induction of MAS.
Published in
STAT1 drives the immune landscape of murine Toll-like receptor 9-induced liver inflammation
De Visscher A, Beliën J, Bernaerts E et al. · JHEP reports : innovation in hepatology 2026 · PMID 41561071 · doi:10.1016/j.jhepr.2025.101668
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Direct links to NCBI, no account and no request form: the whole study as GSE287998_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 8 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1215434 and SRA study SRP559748. Searching any of these in the dataset finder brings you back here.

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