Possible mechanisms of action of the antiphospholipid binding antibodies.
If antibodies directed against the phospholipid itself play any part in the pathogenesis of the thrombotic events, the very ubiquitous nature of the antigen dictates that no single pathogenetic mechanism can be implicated. The majority of in vivo studies recently performed have failed to show that antiphospholipid (aPL) antibodies bind cultured endothelial cells, or that they affect prostacyclin production by these cells. Previously postulated actions showing defective fibrinolysis and impairment of coagulation inhibitors (protein C, thrombomodulin and antithrombin III) have yet to be substantiated. Studies have thus far failed to demonstrate any significant binding of aPL antibodies to intact platelets, although binding to disrupted platelets has been documented.
Khamashta
M A
MA
Lupus Arthritis Research Unit, Rayne Institute, St Thomas' Hospital, London, U.K.
Asherson
R A
RA
Hughes
G R
GR
D000990:Antithrombin III / Q000037:antagonists & inhibitors; D001323:Autoantibodies / Q000502:physiology*; D001792:Blood Platelets / Q000276:immunology; D011464:Epoprostenol / Q000037:antagonists & inhibitors; D005342:Fibrinolysis; D006801:Humans; D010743:Phospholipids / Q000276:immunology*; D011486:Protein C / Q000037:antagonists & inhibitors; D011956:Receptors, Cell Surface / Q000037:antagonists & inhibitors; D018179:Receptors, Thrombin; D013577:Syndrome; D013927:Thrombosis / Q000209:etiology / Q000276:immunology
D001323:Autoantibodies; D010743:Phospholipids; D011486:Protein C; D011956:Receptors, Cell Surface; D018179:Receptors, Thrombin; D000990:Antithrombin III; D011464:Epoprostenol