Vasculitis & polymyalgia rheumatica
CD177 + Neutrophils Promote Endothelial Senescence Through Extracellular Traps in Behçet Disease
Authors' conclusion
Increased CD177+PMN in patients with BD promotes senescence and SASP in VECs through secreting H3.1-enriched NETs, which recruit PMN and collectively contribute to vasculitis in BD.
Study context
- Population
- Patients with Behçet disease (BD) (peripheral blood and vascular tissue) and healthy controls38 BD peripheral samples
- Comparison
- BD CD177+polymorphonuclear neutrophil (PMN) vs healthy control CD177+PMN
Methodological detailsRNA sequencing, mass spectrometry
- RNA sequencing
- Mass spectrometry
Main finding
As reported in the abstract
- BD PMN overexpressed CD177
- CD177+PMN subset expanded in active and severe systemic BD and accumulated in BD aortic walls
- Enhanced NETosis and oxidative phosphorylation in BD CD177+PMN, confirmed in resting and activated cells
- BD CD177+PMN-derived neutrophil extracellular trap (NETs) promoted senescence, senescence-associated secretory phenotype (SASP) and PMN chemotaxis in vascular endothelial cells (VECs) (up-regulated IL-6, CXCL8, ICAM-1, p21, SA-β-gal, cell proliferation arrest)
- BD CD177+PMN-derived NETs contained more histone 3.1 (H3.1)
- H3.1 induced senescence, SASP and PMN chemotaxis in VECs via Toll-like receptor 4 signaling, attenuated by senolytics
Original publication
CD177 + Neutrophils Promote Endothelial Senescence Through Extracellular Traps in Behçet Disease. Arthritis Rheumatol. Published 11 May 2026. doi:10.
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