In vitro characterization of rare anti-αIIbβ3 isoantibodies produced by patients with Glanzmann thrombasthenia that severely block fibrinogen binding and generate procoagulant platelets via complement activation

•Patients with GT may produce anti-αIIbβ3 isoantibodies after platelet transfusions.•Rare anti-αIIbβ3 can block fibrinogen binding and induce procoagulant platelet formation.•Procoagulant platelets induced by complement activation might cause transfusion refractoriness.•Complement directed therapeutic interventions might rescue platelet transfusion efficiency.