INDUCTION OF ENDOTHELIAL-CELL TISSUE FACTOR ACTIVITY BY SERA FROM PATIENTS WITH ANTIPHOSPHOLIPID SYNDROME - A POSSIBLE MECHANISM OF THROMBOSIS

OBJECTIVE: The hypothesis of our study is that antiphospholipid antibodies predispose to thrombosis by inducing endothelial cell tissue factor expression. STUDY DESIGN: Monolayers of cultured human umbilical vein endothelial cells were incubated for 8 hours in a medium containing 20% serum obtained either from patients with antiphospholipid antibodies (n = 11) or normal subjects (n = 8). Similar incubations were performed with immunoglobulin G fractions from either patients with antiphospholipid antibodies (n = 3) or normal subjects (n = 3). Endothelial cell tissue factor expression was measured with a tissue factor-specific chromogenic substrate assay. The results were analyzed with a two-tailed t test. RESULTS: The mean endothelial cell tissue factor expression induced by antiphospholipid sera was significantly greater than the controls (p < 0.02). Immunoglobulin experiments indicated that the factor(s) responsible for the induction of tissue tactor expression resides in the immunoglobulin G traction of the sera (p < 0.01). CONCLUSIONS: Endothelial cell tissue factor expression is induced by antiphospholipid sera, with activity residing at least in part in the immunoglobulin fraction. The induction of tissue factor by antiphospholipid sera may play a role in the thrombotic tendency observed in patients with antiphospholipid syndrome.