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Background: Dimerization of β₂‐glycoprotein I (β₂‐GPI) by autoantibodies is thought to trigger the clinical manifestations observed in the antiphospholipid syndrome. Arterial thrombosis, a frequently occurring clinical manifestation of the antiphospholipid syndrome, is a process in which platelets play a crucial role. Previous work has shown that binding of dimeric β₂‐GPI to the platelet receptors apolipoprotein E receptor 2′ (ApoER2′) and glycoprotein Ibα (GPIbα) mediates increased platelet activation in an in vitro thrombosis model. Objective: The individual roles of ApoER2′ and GPIbα in mediating platelet activation by dimeric β₂‐GPI has hitherto been unclear. In this study, we have determined the roles of either receptor in platelet activation by dimeric β₂‐GPI. Methods: Platelet activation by dimeric β₂‐GPI was studied under conditions of flow. Intracellular signaling induced by dimeric β₂‐GPI was …