Further evidence for the presence of anti-protein S autoantibodies in patients with systemic lupus erythematosus
Résumé
Acquired protein S (PS) deficiency in systemic lupus erythematosus (SLE) has been previously reported, but its mechanism and its possible thrombotic role have not been established. The aim of our study was to provide further evidence for auto-immune PS deficiency in 27 Tunisian SLE patients, using PS-specific enzyme-linked immunosorbent assay (ELISA) and surface plasmon resonance technology (SPR). PS deficiencies for PS activity, free PS or total PS, respectively, were found in 19, 18 and 12 patients. A significant correlation (r= -0.475, P< 0.016) was found between free/total PS ratio and C4bBP levels, suggesting a role of inflammation in free PS deficiency. Immunoglobulin IgG antibodies to PS were detected in four patients by both ELISA and SPR, in six patients only by ELISA, and in two patients only by SPR. Signals for anti-PS IgG by ELISA and SPR were, however, significantly correlated (r = 0.549, P = 0.003). These results suggest that an auto-immune mechanism could account for low PS activity in patients with SLE. Auto-antibodies to PS may form immune complexes, inducing increased clearance of PS or interfering with the protein C-protein S system.