Background The complement system plays an important role in systemic lupus erythematosus (SLE) and it might be a therapeutic target for therapy. Type I interferon (IFN) response and type I IFN-induced gene expression are generally enhanced in SLE. Therefore, it was suggested that type I IFN response played a role in SLE pathogenesis.

Objectives We evaluated some biomarkers associated with type I IFN response and complement activation in SLE; and determined their relationship with clinical findings.

Methods We included 94 SLE patients (88 females, 6 males, mean age: 39 years) and 101 healthy controls (87 females, 14 males, mean age: 38 years). SLE patients' clinical and laboratory data were obtained from medical records. Complement factor H, complement fragments Bb, C3a-des-arg, ficolin-2, sCXCL-12 (plasma stromal cell derived factor, SDF-1), sCXCL-10 (IP-10), neutrophil activation-related LL-37, and BLyS levels were determined with ELISA kits.

Results SLE patients had significantly higher sCXCL-12 (646.9±859.1 vs. 242.8±240.8, p=0.001), sCXCL-10 (469.6±537.9 vs. 262.9±351.4, p=0.012), and complement fragments Bb (4.36±2.2 vs 3.68±2.5, p=0.046) levels than healthy controls. C3a-des-arg (4.14±2.2 vs. 4.94±1.4, p=0.003) and LL-37 (3.74±1.8 vs. 5.5±1.6, p<0.001) levels were significantly lower in SLE group than in the control group. Ficolin-2 and BLyS levels were similar in both groups. When SLE patients whose SLEDAI scores were active and inactive were compared, it was seen that sCXCL-10 was significantly higher in the former group (p=0.023). SLE patients with arthritis had significantly higher sCXCL-12 (p=0.003), BLyS (p=0.03), sCXCL-10 (p=0.001) and complement fragments Bb (p=0.004) levels than SLE patients without arthritis. SLE patients with neurologic involvement had significantly lower C3a-des-arg level when compared to other SLE patients (3.23±1.56 vs 4.43±2.04, p=0.022). C3a-des-arg level was significantly higher in SLE patients with thrombocytopenia than SLE patients without thrombocytopenia (5.44±2.64 vs 4.03±1.98, p=0.043). sCXCL-10 correlated with SLEDAI score (r=0.33, p=0.014), disease duration (r=0.26, p=0.05), and BLyS level (r=0.59, p<0.001). BLyS was found to correlate with LL-37 (r=0.27, p=0.033) and disease duration (r=0.39, p=0.002). Complement fragment Bb correlated with CRP level (r=0.3, p=0.005).

Conclusions Our results support the roles of type I IFN response and complement activation in the pathogenesis of SLE. sCXCL-12, sCXCL-10, C3a-des-arg, LL-37, and complement fragments Bb might be used as biomarkers in SLE and they might be useful to define certain clinical subgroups.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.3752