Por favor, use este identificador para citar o enlazar este ítem: https://hdl.handle.net/10495/29425
Título : Endothelial cell-derived extracellular vesicles released upon stimulation with antiphospholipid antibodies: A genuine direct procoagulant mechanism or a new factor in the lupus anticoagulant paradox?
Autor : Álvarez Jaramillo, Daniel
Rúa Molina, Diana Carolina
Velásquez Berrío, Manuela
Cataño Bedoya, John Ubeimar
Escudero, Carlos
Cadavid Jaramillo, Ángela Patricia
metadata.dc.subject.*: Inhibidor de Coagulación del Lupus
Lupus Coagulation Inhibitor
Anticuerpos Antifosfolípidos
Antibodies, Antiphospholipid
Trombosis
Thrombosis
Síndrome Antifosfolípido
Antiphospholipid Syndrome
metadata.dc.contributor.conferencename: Latino American and Caribbean Congress of Immunology (13 : 7 de junio de 2022 : Varadero, Cuba)
Fecha de publicación : 2022
Resumen : ABSTRACT: Background: Antiphospholipid antibodies (aPL) are a heterogeneous group of autoantibodies that lead to thrombosis and pregnancy morbidity. Paradoxically, the capacity of some of these autoantibodies to inhibit coagulation pathways in vitro relates to their capacity to trigger thrombosis in vivo. While the exact mechanism(s) by which aPL dampen clotting in vitro remains to be demonstrated, it is known that aPL activate endothelial cells thus triggering the production of presumably procoagulant extracellular vesicles (EVs). Aim: To assess the procoagulant activity of endothelial cell-derived extracellular vesicles released by aPL stimulus. Results: IgG from patients with primary vascular and obstetric APS who manifest refractoriness to treatment, lead to a prolongation in lag time and a decrease in overall coagulation potential related to EV-rich supernatant of endothelial cells. This effect is abrogated by co-stimulation of endothelial cells with β2GPI, cannot be explained by changes in the number of EVs, and is not shared with IgG from patients with obstetric or vascular clinical manifestations alone, IgG from non-refractory patients even with both clinical conditions or IgG from patients with aPL-non-related clinical manifestations. Conclusions: According to our knowledge, for the first time we are describing that anticoagulant effects of some aPL are reflected in the endothelial cell-derived EVs for which the same autoantibodies perform as triggers. Our findings suggest that EVs do not constitute a direct procoagulant mechanism. Further analysis is required to establish how this phenomenon relates to lupus anticoagulant and whether aPL from patients with the worst clinical features make up immunocomplexes with EVs.
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