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Serum concentrations of IL-17A, IL-17B, IL-17E and IL-17F in patients with systemic sclerosis.
Archives of Medical Science : AMS 2019 May
Introduction: Immune system activation, microvascular abnormalities and extracellular matrix deposition in tissues play roles in systemic sclerosis (SSc). Th17 cells producing interleukin (IL)-17 are involved in the pathogenesis of many autoimmune-mediated inflammatory diseases; however, the role of IL-17 in SSc remains unclear.
Material and methods: The concentrations of IL-17A, IL-17B, IL-17E, and IL-17F in the serum of patients with SSc and in the healthy control group were assessed with regard to type of the disease - whether limited (lSSc) or diffuse (dSSc) - and symptoms.
Results: No difference was found between patients with SSc and the control group as regards the serum concentration of IL-17A. However, IL-17B and IL-17E levels in patients with SSc, and its types diffuse and limited were higher ( p < 0.001) compared to the control. The serum level of IL-17F was higher in SSc ( p < 0.005) and lSSc ( p < 0.05) compared to the control. Serum concentration of IL-17B was elevated in SSc patients with renal abnormalities ( p < 0.05) compared to those without. Serum levels of IL-17B correlated with the levels of IL-17E in patients with SSc ( r = 0.54, p < 0.05).
Conclusions: Increased synthesis of IL-17B, IL-17E and IL-17F appears to play a role in the pathogenesis of SSc, in contrast to IL-17A. Higher levels of IL-17B and IL-17E are associated with the development of both lSSc and dSSc, whereas IL-17F is associated with lSSc only. Further studies are needed to elucidate their role in the pathogenesis of the disease.
Material and methods: The concentrations of IL-17A, IL-17B, IL-17E, and IL-17F in the serum of patients with SSc and in the healthy control group were assessed with regard to type of the disease - whether limited (lSSc) or diffuse (dSSc) - and symptoms.
Results: No difference was found between patients with SSc and the control group as regards the serum concentration of IL-17A. However, IL-17B and IL-17E levels in patients with SSc, and its types diffuse and limited were higher ( p < 0.001) compared to the control. The serum level of IL-17F was higher in SSc ( p < 0.005) and lSSc ( p < 0.05) compared to the control. Serum concentration of IL-17B was elevated in SSc patients with renal abnormalities ( p < 0.05) compared to those without. Serum levels of IL-17B correlated with the levels of IL-17E in patients with SSc ( r = 0.54, p < 0.05).
Conclusions: Increased synthesis of IL-17B, IL-17E and IL-17F appears to play a role in the pathogenesis of SSc, in contrast to IL-17A. Higher levels of IL-17B and IL-17E are associated with the development of both lSSc and dSSc, whereas IL-17F is associated with lSSc only. Further studies are needed to elucidate their role in the pathogenesis of the disease.
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