Lupus & antiphospholipid syndrome
CD40-CD40L inhibition attenuates platelet-neutrophil interaction and neutrophil extracellular trap release in primary antiphospholipid syndrome
Authors' conclusion
Targeting the platelet-neutrophil/autophagy/TF-expressing NETs axis by CD40-CD40L inhibition attenuates thromboinflammation in PAPS
Study context
- Population
- Patients with primary antiphospholipid syndrome (PAPS), asymptomatic aPL carriers and healthy controls (HCs); venous thrombosis mouse model
- Comparison
- PAPS vs asymptomatic aPL carriers vs healthy controls; CD40-CD40L inhibition vs none
- Outcome
- NET release and mechanisms driving NET formation and thrombogenic effects of NETs in PAPS
Methodological detailsin vitro, venous thrombosis mouse model, human tissue immunofluorescence
- In vitro
- Venous thrombosis mouse model
- Human tissue immunofluorescence
Main finding
As reported in the abstract
- PAPS neutrophils showed increased NET release vs asymptomatic aPL carriers and HCs
- Neutrophil extracellular traps (NETs) from PAPS expressed tissue factor (TF) that induced thrombin generation in platelet-poor plasma from HCs
- aPL induced in vitro intracellular TF expression in HC neutrophils
- TF-expressing NETs abundant in kidney, skin ulcer and endoarterial thrombus tissues from PAPS, colocalised with fibrinogen
- NET release in PAPS driven by aPL-mediated platelet activation, platelet-neutrophil interaction and autophagy induction
- CD40-CD40L blockade reduced platelet activation, autophagy and NET formation in PAPS
- In mice, CD40-CD40L inhibition reduced neutrophil-platelet aggregates and MPO-DNA complexes in peripheral blood, and NETs in formed thrombi
Original publication
CD40-CD40L inhibition attenuates platelet-neutrophil interaction and neutrophil extracellular trap release in primary antiphospholipid syndrome. Ann Rheum Dis. Published 21 January 2026. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →