Measurement of Serum Fas Ligand (FasL), FasL-Fas Complex and FasL-IgG Complex in Patients with Rheumatic Diseases / 대한류마티스학회지

ABSTRACT

OBJECTIVE: To quantify the soluble Fas ligand (sFasL) and to measure FasL-Fas complex and FasL-IgG complex in the sera of patients with various rheumatic diseases systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), systemic sclerosis (SSc), and adult onset Still? disease (AOSD). METHODS: Serum samples were obtained from 37 patients with SLE, 40 with RA, 30 with SSc, 20 with AOSD, and 40 healthy controls. The serum sFasL, FasL-Fas complex, and FasL-IgG complex were measured using a sandwich enzyme-linked immunoabsorbent assay. Hospital medical records were retrospectively reviewed for clinical and laboratory characteristics in patients with SLE. Disease activity in SLE patients was assessed by the SLE Disease Activity Index (SLEDAI) score. RESULTS: In patients with SLE, serum sFasL levels (383.1+/-208.9pg/ml) were significantly higher (p<0.001) than those of healthy controls (192.0+/-84.7pg/ml). sFasL levels in patients with RA (150.8+/-30.7pg/ml, p=0.014), SSc (115.4+/-13.5pg/ml, p<0.001), and AOSD (137.5+/-12.9pg/ml, p=0.001) were significantly lower compared with healthy controls. The frequencies of positive FasL-Fas complex and FasL-IgG complex were higher in patients with SLE (56.8%, 56.8% respectively) than in healthy controls (2.5%, 0% respectively) (p<0.001). All patients with RA or AOSD were negative for FasL-Fas complex and FasL-IgG complex. No patients with SSc were positive for FasL-Fas complex. On the other hand, the positive frequency of FasL-IgG complex was greater in patients with SSc (16.7%) than in healthy controls (0%)(p=0.012). Serum levels of FasL-IgG complexes in active SLE patients (OD 0.467+/-0.050) were tended to be lower than those in inactive SLE patients (OD 0.509+/-0.055)(p=0.060). SLEDAI score was tended to be negatively correlated with the serum levels of FasL-IgG complex in patients with SLE (r=-0.308, p=0.068). CONCLUSION: These results suggest that FasL may possibly play a role in the pathogenesis of SLE.