Lupus & antiphospholipid syndrome
Differential complement pathways and components in the clinical spectrum of systemic lupus erythematosus
Authors' conclusion
The CP is predominantly activated at disease onset, whereas the AP contributes to both initiation and progression of SLE.
Study context
- Population
- Patients with systemic lupus erythematosus (SLE) and healthy controls
- Participants
- 60 vs 20
- Exposure
- SLE patients vs healthy controls; active vs low disease activity SLE
- SLEn = 60
- Healthy controls (HC)n = 20reference
- Outcome
- Plasma complement pathway components (C1q, C4, C4b, C2, C3, C5, FB, FP, FD, FH, Factor I (FI), Mannose-binding lectin)
Methodological detailsMultiplex Assay of plasma complement components
- Multiplex Assay of plasma complement components
Main finding
As reported in the abstract
Complement components by disease activity
- Active SLE vs HC and low disease activity: decreased C1q, C4, C4b, C3 and Factor P (FP), increased C2; Factor B (FB) reduced only vs HC
- Low C3 and C4: higher anti-dsDNA and C2, more newly diagnosed SLE, lower C1q, C5, FP, FB and Factor H (FH)
- Isolated low C3: reduced FP, FB and FH, trend toward longer disease duration
- Newly diagnosed SLE: decreased C1q and C4b
- Renal involvement: lower C1q and C3, higher C2
- Concurrent infection: decreased C1q, increased C2
- Regression: C2 independently associated with concurrent infection; Factor D (FD) strongest negative correlation with renal function
- Principal component analysis: three patient clusters with distinct complement signatures
Observational data: associations, not effects.
Original publication
Differential complement pathways and components in the clinical spectrum of systemic lupus erythematosus. Arthritis Res Ther. Published 26 December 2025. doi:10.
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