Abstract

The pathogenesis of the immunoglobulin A vasculitis (IgAV) is still unknown. The available data shows that interleukin (IL)-17, IL-18, IL-23, regulated on activation, normal T cell expressed and secreted (CCL 5, RANTES), and interferon (IFN)-γ-inducible protein 10 (IP10) participate in the pathogenesis of IgAV by influencing the recruitment of leukocytes to the site of inflammation. The aim of this study was to analyze the serum concentration of IL-17A, IL-18, IL-23, RANTES, and IP10 in patients with acute IgAV compared to healthy children. Moreover, we wanted to assess the suitability of the levels of tested cytokines to predict the severity of the disease. All children with IgAV hospitalized in our institution between 2012 and 2017 were included in the study. Cytokines levels were determined in a serum sample secured at admission to the hospital. Basic laboratory tests have also been analyzed. IL-17A, IL-18, and IL-23 were significantly higher in whole IgAV group (52.25 pg/ml; 164.1 pg/ml and 700 pg/ml, respectively) than in the control group (27.92 pg/ml; 140.1 pg/ml and 581.5 pg/ml, respectively). The receiver operating characteristic (ROC) curve analysis revealed the largest area under the curve (AUC 0.979, p < 0.001) for the IL-17A with 95.1% sensitivity and 91.7% specificity. There were no significant differences in cytokine levels depending on the severity of the IgAV. Although the serum levels of the IL-17A, IL-18, and IL-23 increase significantly in the acute phase of the IgAV, they cannot be used as indicators of predicting the course of the disease. IL-17A seems to be a good predictor of IgAV occurrences.

Highlights

  • Immunoglobulin A vasculitis (IgAV), formerly known as Henoch–Schonlein purpura, is the most common systemic vasculitis in childhood with a reported incidence of 3–26.7/100 000 [1]

  • We showed significant differences in the levels of IL-17A, IL-18, and IL-23 between the groups studied

  • The significantly higher serum level of mentioned cytokines in children with acute IgAV may confirm their participation in the pathogenesis of the disease

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Summary

Introduction

Immunoglobulin A vasculitis (IgAV), formerly known as Henoch–Schonlein purpura, is the most common systemic vasculitis in childhood with a reported incidence of 3–26.7/100 000 [1]. The importance of the autoimmune hypothesis of the pathogenesis of the disease increased significantly [2, 3]. Taking new reports into account, the view on the pathogenesis of autoimmune diseases has changed, and the Th1 lymphocytes (Th1)/Th2 lymphocytes (Th2) paradigm is in decline. Th2 stimulate mainly the humoral immune response, the production of IgA, IgE, IgG4 antibodies, as well as the growth and differentiation of mast cells and eosinophils.

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