ArticleHaematologica2026
Mechanisms sensitive to different drugs mediate a proadhesive and pro-thrombotic platelet phenotype in antiphospholipid syndrome.
Article in Haematologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Anti-phospholipid antibodies (aPL) mediate platelet- and leukocyte-interaction with damaged endothelium, contributing to anti-phospholipid syndrome (APS) vasculopathy. This study aimed to understand the mechanisms sustaining the pro-adhesive/- thrombotic platelet phenotype and the in vitro effects of different drugs. We included 34 primary APS (PAPS) patients and 12 healthy subjects (HS). All patients had medium/high aPL levels with vascular/obstetric symptoms according to the 2023 ACR/EULAR classification. In vivo, we evaluated by flowcytometry platelet activation markers (P-selectin, activated GPIIbIIIa [aGPIIbIII], tissue factor [TF], ApoER2 and β2GPI expression and platelet-monocyte and -granulocyte aggregates [PMA and PGA]). In vitro, the impact of antiplatelet and anti-inflammatory drugs on platelet activation induced by different aPL subpopulations was investigated. PAPS patients exhibited greater percentages of circulating ApoER2pos-, P-selectinpos-, aGPIIbIIIapos-, TFpos-platelets, and TFpos-platelet-leukocyte aggregates. In vitro, HS blood incubation with PAPS plasma fully reproduced the activation found in vivo. While anti-β2GPI-Domain(D)1, but not anti-D4,5, immunoglobulin (Ig)G upregulated platelet TF expression only, the addition of interleukin (IL)-6 also induced P-selectin and aGPIIbIIIa upregulation. An IL-6 receptor-blocking monoclonal antibody prevented the pro-adhesive/-coagulant platelet phenotype and the formation of platelet-leukocyte aggregates mediated by PAPS plasma or by total IgG plus exogenous IL-6. While aspirin and P2Y12 inhibitor fully inhibited platelet activation, hydroxychloroquine (HCQ) did not blunt TF expression. PAPS patients exhibit circulating pro-adhesive/-coagulant (TF-positive) platelets and platelet-leukocyte aggregates mediated by β2GPI-D1-dependent IgG and an inflammatory trigger. While aspirin and P2Y12 inhibitor significantly inhibited the aPL-mediated P-Selectin and TF upregulation, HCQ affected the adhesion phenotype only, and might not be adequate to prevent platelet-mediated thrombosis.
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