Autoinflammatory & rare systemic diseases
A Multifaceted Interplay Among Hemophagocytosis, Interleukin‐18, and Type I Interferon Distinguishes Still Disease From Other Autoinflammatory Diseases
Authors' conclusion
This unprecedented large omics data set of SAIDs revealed that complex interactions among hemophagocytosis, IL-18, and type I IFN signaling characterize SD. Furthermore, two distinct subgroups in patients with SD were distinguished by the degree of hemophagocytic activity.
Study context
- Population
- Patients with systemic autoinflammatory diseases (SAID)
- Participants
- 372 patients
- Comparison
- SD vs non-SD SAIDs
- SDn = 72
- Non-SD SAIDsn = 300reference
Methodological detailsSomaScan proteomics, RNA sequencing (RNA-Seq), ELISA validation, weighted gene correlation network analysis
- SomaScan proteomics
- RNA-Seq
- ELISA validation
- Weighted gene correlation network analysis
Main finding
As reported in the abstract
- Elevated plasma HO-1 and IL-18 strongly correlate and characterize SD but do not associate with general inflammation
- SD characterized by ferroptosis in plasma, type I interferon (IFN) signaling in monocyte transcriptomes, and elevated NK cell miRNA-146a-5p (an IL-18 induced microRNA (miRNA))
- Feature modules distinguish SD from other SAIDs and stratify SD into two distinct subgroups not attributable to disease activity or inflammation but hemophagocytosis
Original publication
A Multifaceted Interplay Among Hemophagocytosis, Interleukin‐18, and Type I Interferon Distinguishes Still Disease From Other Autoinflammatory Diseases. Arthritis Rheumatol. Published 8 April 2026. doi:10.
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