ArticleArchives of medical science : AMS2026
Interplay between IL-17 family members and angiogenic cytokines in subjects with systemic sclerosis.
Article in Archives of medical science : AMS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors.
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Abstract
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; 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.
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