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Low ectonucleotidase activity and increased neutrophil-platelet aggregates in patients with antiphospholipid syndrome
Somanathapura K NaveenKumar1, Ajay Tambralli1,2, Bruna Mazetto Fonseca1,3
1Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI.
Many patients with antiphospholipid syndrome had decreased ectonucleotidase activity on neutrophils and platelets, which enabled extracellular nucleotides to trigger neutrophil-platelet aggregates. This phenotype was replicated by treating healthy neutrophils and platelets with patient-derived antiphospholipid antibodies or ectonucleotidase inhibitors.
Many patients with antiphospholipid syndrome had decreased ectonucleotidase activity on neutrophils and platelets, which enabled extracellular nucleotides to trigger neutrophil-platelet aggregates. This phenotype was replicated by treating healthy neutrophils and platelets with patient-derived antiphospholipid antibodies or ectonucleotidase inhibitors.
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