Autoinflammatory & rare systemic diseases
Targeting neutrophil-driven inflammation in adult-onset still’s disease: molecular insights from gene expression profiles
Authors' conclusion
Neutrophil activation is a key pathological module in AOSD.
Study context
- Population
- Blood transcriptomic dataset of patients with adult-onset Still's disease (AOSD) and healthy controls
- Participants
- 31 vs 22
- Comparison
- AOSD vs healthy controls
- AOSDn = 31
- Healthy controlsn = 22reference
- Outcome
- Blood molecular signatures and molecular targets for neutrophil activation
Methodological detailsblood transcriptomic dataset, differentially expressed genes and functional enrichment analysis, kernel-based diffusion scoring
- Blood transcriptomic dataset
- Differentially expressed genes and functional enrichment analysis
- Kernel-based diffusion scoring
Main finding
As reported in the abstract
- Neutrophil degranulation is the most enriched pathological process in AOSD
- Neutrophil degranulation correlated significantly with expression of Fcγ receptors, IL-1 receptors and chemokine receptors and their signalling activities
- IL-1 inhibitors and IL-6 inhibitors did not show a diffusion score favourable for directly deactivating neutrophil degranulation
- Agents targeting CXCR1/CXCR2, C5AR1, neutrophil elastase, SRC and SYK showed significant diffusion scores for neutrophil degranulation
- CXCR1, CXCR2 and C5AR1 were differentially expressed genes (DEGs) predominantly expressed in neutrophils and closely associated with neutrophil degranulation in context-specific functional analysis
Original publication
Targeting neutrophil-driven inflammation in adult-onset still’s disease: molecular insights from gene expression profiles. Arthritis Res Ther. Published 1 July 2025. doi:10.
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