Pathogenesis of the antiphospholipid antibody syndrome.
Review
Overview
abstract
Endothelial and/or platelet activation likely initiates thrombus formation. Whether antiphospholipid antibody (aPL) is an activator, a toxic response, or a protective response is not clear, nor is it certain whether aPL is germ-line encoded or antigen-driven. The pregnancy model is particularly informative. Alternative hypotheses about thrombogenicity which relegate aPL to the role of bystander have not yet been excluded.
