Abstract
Expression of tissue factor activity on cells in contact with flowing blood is the trigger for physiological coagulation as well as many types of thrombosis. A number of older observations and considerable recent data suggest that increased tissue factor activity is an important cause of hypercoagulability in the antiphospholipid syndrome. Potential mechanisms contributing to upregulation of the tissue factor pathway include increased expression of tissue factor due to increased transcription, increased functional activity of tissue factor molecules due to de-encryption and decreased activity of tissue factor pathway inhibitor. Autoantibodies and/or immune complexes appear to play a major role in enhanced tissue factor activity, although increased levels of inflammatory cytokines may also contribute. Anti-beta 2-glycoprotein I autoantibodies have been specifically implicated in the antibody-mediated enhancement of tissue factor activity.