Pathogenesis of the antiphospholipid antibody syndrome.
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.
Lockshin
M D
MD
Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892, USA.
D000022:Abortion, Spontaneous / Q000209:etiology; D016736:Antiphospholipid Syndrome / Q000209:etiology*; D001792:Blood Platelets / Q000502:physiology; D004730:Endothelium, Vascular / Q000166:cytology; D005260:Female; D006801:Humans; D011247:Pregnancy