Complement Activation Linked to Type II Interferon Signaling in Still Disease
Authors' conclusion
SD is characterized by complement activation with marked up-regulation of C1q, which is closely linked to IFN-γ/type II signaling.
Study context
- Population
- Patients with Still disease (onset/active and remission/inactive), nonsystemic juvenile idiopathic arthritis (JIA), macrophage activation syndrome and healthy donors
- Participants
- 15 / 8 / 19 / 18 / 2
- Comparison
- Still disease (onset/active) vs remission/inactive SD, nonsystemic JIA and healthy donors
- Healthy donorsn = 15
- Nonsystemic JIAn = 8
- SD at onsetn = 19
- SD remissionn = 18reference
- Macrophage activation syndromen = 2
- Outcome
- Complement activation in SD
Methodological detailstranscriptomic, proteomic and in vitro approaches
- Transcriptomic, proteomic and in vitro approaches
Main finding
As reported in the abstract
- Classical complement genes (C1QB/C1QC) markedly up-regulated in onset SD vs remission SD and JIA
- Active SD: increased C1q, C3a, C5a and terminal complement complex protein levels, with enhanced functional classical complement activity
- Whole-blood C1QB/C1QC expression correlated with interferon (IFN)-related markers, including IL-18, CXCL9 and CXCL10
- Recombinant IFN-γ induced monocytic C1q; C1q enhanced IFN-γ production by CD8+ T cells (feed-forward loop)
- SD at onset vs SD remission: adjusted P = 3.7 × 10-36
Original publication
Complement Activation Linked to Type II Interferon Signaling in Still Disease. Arthritis Rheumatol. Published 25 August 2026. doi:10.
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