Lupus & antiphospholipid syndrome
Imbalance between serum DNase-I protein levels and enzymatic activity in SLE: link with mitochondrial-DNA and low-density granulocytes
Authors' conclusion
The DNase-I levels vs enzymatic activity imbalance in SLE may be influenced by elevated anti-DNase-I antibodies and diminished pGSN concentrations, collectively impairing cirDNA degradation and promoting anti-DNA autoantibody production.
Study context
- Population
- SLE patients and controls
- Participants
- 144 vs 42
- Exposure
- SLE patients vs controls
- SLEn = 144
- Controlsn = 42reference
- Outcome
- Role of DNase-I and its main regulatory factors controlling cirDNA degradation, in relation to LDG subsets in SLE
Methodological detailscase-control
- Case-control
Main finding
As reported in the abstract
- Serum DNase-I levels increased in SLE without a concomitant increase in DNase activity, particularly among anti-dsDNA-positive patients, who also had the highest cirDNA concentrations
- Anti-DNase-I antibody levels elevated in these patients and positively correlated with the DNase-I/cirDNA ratio
- Plasma gelsolin (pGSN) levels reduced in active patients or with CVD; higher pGSN associated with fewer CD16neg-LDG (atherogenic subset)
- CD16pos-LDG increased in SLE and inversely associated with DNase activity; mtDNA may contribute to their generation
- In controls, mtDNA correlated with circulating DNase-I levels and activity
Observational data: associations, not effects.
Original publication
Imbalance between serum DNase-I protein levels and enzymatic activity in SLE: link with mitochondrial-DNA and low-density granulocytes. Rheumatology (Oxford). Published 3 November 2025. doi:10.
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