Deletion of the antiphospholipid syndrome autoantigen β2 -glycoprotein I potentiates the lupus autoimmune phenotype in a Toll-like receptor 7-mediated murine model.

Objective: The BXSB.Yaa mouse strain is a model of systemic lupus erythematosus that is dependent on duplication of the Toll-like receptor 7 gene. The objective of this study was to systematically describe the amplified autoimmune phenotype observed when the soluble plasma protein β2 -glycoprotein I (β2 GPI) gene was deleted in male BXSB.

Post-translational oxidative modification of β2-glycoprotein I and its role in the pathophysiology of the antiphospholipid syndrome.

Vascular thrombosis and/or recurrent miscarriages are the main characteristics defining Antiphospholipid Syndrome (APS). Currently there is no well-defined clinical features and/or laboratory tests that predicts the risk of adverse prognostic outcomes in APS. In this short review, we report the importance of posttranslational modification of beta2 glycoprotein I, the major autoantigen in the APS beta2 glycoprotein I that may, in part, explain possible mechanisms for the generation of auto antibodies to beta2 glycoprotein I.

New insights into the biology and pathobiology of beta2-glycoprotein I.

β2-glycoprotein I (β2GPI) is the major autoantigen in the antiphospholipid syndrome. The central importance of understanding β2GPI physiology from the perspective of the rheumatologist is that it forms the foundation for understanding the pathophysiology underlying autoantibody generation, and the diverse mechanisms by which anti-β2GPI antibodies in complex with β2GPI may predispose an individual to the antiphospholipid syndrome clinical phenotype. This review examines some of the latest novel findings in this area.