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FRI0391 The Association between Type I Interferon Response, Complement Activation and Clinical Findings in Systemic Lupus Erythematosus
  1. K. Sacar1,
  2. O.N. Pamuk2,
  3. G.E. Pamuk3,
  4. M.S. Uyanik3,
  5. S. Donmez1
  1. 1Rheumatology, Trakya University Medical Faculty, Edirne
  2. 2Rheumatology, Trakya University Medical Faculty, Istanbul
  3. 3Hematology, Trakya University Medical Faculty, Edirne, Turkey

Abstract

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

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