A toggle switch linking coagulation and innate immunity in antiphospholipid antibody syndrome

Abstract

The antiphospholipid syndrome (APS) is defined by the occurrence of thrombotic events or adverse pregnancy outcomes in individuals who persistently test positive for antiphospholipid antibodies (aPLs), including anticardiolipin antibodies, lupus anticoagulant, and anti–β2-glycoprotein 1 antibodies. A range of clinical features can occur in the context of APS, with thrombotic manifestations potentially occurring in any vessels, arterial or venous, large vessels, or microvasculature.1 Previous studies have shown that aPLs induce translocation of toll-like receptors (TLRs) 7 and 8 to the endosome, promoting proinflammatory signaling.