Lupus & antiphospholipid syndrome
Neutrophils impaired by anti-galectin-3 antibodies elicit inflammation of endothelial cells to aggregate the development of lupus cutaneous vasculitis
Authors' conclusion
Overall, these findings suggested that neutrophils were crucial mediators in anti-Gal3 Ab induced lupus cutaneous vasculitis.
Study context
- Population
- SLE patients and healthy controls (HCs); neutrophils stimulated by patient or HC serum or anti-Gal3 Ab; human umbilical vein endothelial cells; lupus skin lesions
Main finding
As reported in the abstract
- Serum anti-Gal3 Ab levels negatively correlated with peripheral neutrophil counts
- Anti-Gal3 Ab positive SLE sera accelerated neutrophil death, altered cell phenotype and promoted NET formation, involving the p38 MAPK pathway
- Supernatants of neutrophils co-cultured with anti-Gal3 Ab provoked endothelial cells to produce cytokines such as IL-1, ICAM-1, SELE and particularly IL-6
- IL-6 higher in SLE patients with anti-Gal3 Ab positive sera and enriched in areas of vascular inflammation, with enhanced Gal3 expression and neutrophil infiltration
Original publication
Neutrophils impaired by anti-galectin-3 antibodies elicit inflammation of endothelial cells to aggregate the development of lupus cutaneous vasculitis. Clin Exp Rheumatol. Published 7 January 2024. doi:10.
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