Interplay between IL-17 family members and angiogenic cytokines in subjects with systemic sclerosis.

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.