Abstract & Overview
Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by recurrent life-threatening blood clots and pregnancy complications in individuals with antiphospholipid antibodies. Among these antibodies, those targeting the plasma glycoprotein β 2 -glycoprotein I (β 2 GPI) hold particular clinical significance. Despite extensive research, controversies persist regarding the structure of β 2 GPI, which has substantial implications for understanding autoantibody reactivity and APS development. This article critically examines recent advancements in the structural biology of β 2 GPI and its relevance to the recognition of antiphospholipid antibodies. Additionally, it introduces a new structure-based theory to explain how autoantibodies interact with β 2 GPI and the functional consequence of this interaction. Finally, it identifies potential areas for future research that could enhance approaches to diagnosing and treating APS.