Introduction:
Systemic sclerosis (SSc) is a chronic, autoimmune connective tissue disease characterized by immune system activation, vasculopathy, and collagen accumulation. Despite progressive fibrosis of the vasculature, compensatory angiogenesis is impaired. The cause of the shift towards anti- angiogenesis observed in SSc is unknown. The interleukin-17 (IL-17) cytokine family participates in the pathogenesis of SSc and angiogenesis.

Material and methods:
Our study aimed to evaluate levels and find relationships between the levels of proangiogenic cytokines and cytokines from the IL-17 family in 42 SSc subjects and 20 healthy controls. Vascular endothelial growth factor (VEGF), placental growth factor (PlGF), hepatocyte growth factor (HGF), transforming growth factor β1 (TGF-β1), granulocyte/macrophage colony-stimulating factor (GM-CSF), IL-17A, IL-17B, IL-17E and IL-17F were quantified in the sera of all participants by ELISA sandwich kits.

Results:
Significantly higher mean concentrations of PlGF compared to the control mean value (19.3 pg/ml in the SSc group vs. 11.4 pg/ml in the control group; p < 0.001) and of HGF (1931 pg/ml in the SSc group vs. 1483 pg/ml in controls; p < 0.05) were observed. Mean serum TGF-β1 level was also significantly lower in the SSc group (781 pg/ml) than in controls (35991 pg/ml; p < 0.001). Among the IL-17 family, significantly higher mean concentrations of IL-17B (67.0 pg/ml vs. 2.6 pg/ml in controls; p < 0.001), IL-17E (8.0 pg/ml vs. 0.64 pg/ml in controls; p < 0.001) and IL-17F (0.42 pg/ml vs. 0.0 pg/ml in controls; p < 0.01) were detected. Serum concentrations of HGF and PlGF correlated with the concentrations of IL17A, IL-17B, and IL-17E.

Conclusions:
Our findings indicate that selected cytokines from the IL-17 family participate in the pathogenesis of SSc and are responsible for the vascular abnormalities associated with this disorder.