Increased serum interleukin-17 and peripheral Th17 cells in children with acute Henoch-Schönlein purpura

Pediatr Allergy Immunol. 2011 Dec;22(8):862-8. doi: 10.1111/j.1399-3038.2011.01198.x. Epub 2011 Sep 19.

Abstract

Background: Interleukin (IL)-17 and Th17 cells have been involved in many autoimmune diseases. The aim of this study is to investigate the involvement of IL-17 and Th17 cells in the pathogenesis of childhood Henoch-Schönlein purpura (HSP).

Methods: Serum and supernatant levels of cytokines and chemokines were analyzed by enzyme-linked immunosorbent assay (ELISA). Using intracellular staining, the frequency of peripheral Th17 and Th1 cells was studied by flow cytometry.

Results: Children with acute HSP had significantly higher serum levels of IL-17, IL-6 and transforming growth factor-β than healthy controls. The IL-17 levels in culture supernatants of peripheral blood mononuclear cells with anti-CD3 and CD28 antibody stimulation were much higher in patients with HSP (281.2 ± 91.4 vs. 47.7 ± 22.6 pg/ml, p = 0.022). The patients also had more Th17 cells (1.67 ± 0.36% vs. 0.71 ± 0.15%, p = 0.033) but not Th1 cells in peripheral blood. Moreover, IL-17 could promote human endothelial cells to produce chemoattractants IL-8 and monocyte chemotactic protein-1.

Conclusion: The increased frequency of peripheral Th17 cells and serum IL-17 levels are shown in childhood HSP that may in part contribute to vascular inflammation, suggesting cellular immunity is likely to be involved in the process of HSP.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Adolescent
  • Cell Separation
  • Cells, Cultured
  • Chemokine CCL2 / metabolism
  • Child
  • Child, Preschool
  • Endothelial Cells / immunology
  • Endothelial Cells / metabolism
  • Endothelial Cells / pathology
  • Female
  • Flow Cytometry
  • Gene Expression Regulation / immunology
  • Humans
  • IgA Vasculitis / blood*
  • IgA Vasculitis / immunology*
  • Immunization
  • Interleukin-17 / blood*
  • Interleukin-6 / genetics
  • Interleukin-6 / immunology
  • Interleukin-6 / metabolism*
  • Male
  • Th1 Cells / immunology
  • Th17 Cells / immunology*
  • Transforming Growth Factor beta / genetics
  • Transforming Growth Factor beta / immunology
  • Transforming Growth Factor beta / metabolism*

Substances

  • Chemokine CCL2
  • Interleukin-17
  • Interleukin-6
  • Transforming Growth Factor beta