• Rheumatol. Int. · Dec 2012

    Investigation of the change in CD4⁺ T cell subset in children with Henoch-Schonlein purpura.

    • Yuan-Yuan Li, Cheng-Rong Li, Guo-Bing Wang, Jun Yang, and Ying Zu.
    • Institute of Pediatrics, Affiliated Shenzhen Children's Hospital, Chongqing Medical University, Shenzhen 518026, China.
    • Rheumatol. Int. 2012 Dec 1; 32 (12): 3785-92.

    AbstractHelper T (Th) cells comprising Th1, Th2, Th17, and Treg are involved in the pathogenesis of various vascular inflammations, and information about Th cells in Henoch-Schonlein purpura (HSP) is still controversial. The aim of our study was to investigate the changes in CD4(+) T cell subsets and their roles in the pathogenesis of HSP. Thirty children with diagnosis of HSP and thirty age-matched healthy controls were enrolled in this study. Real-time PCR was used to evaluate the mRNA expression levels of transcriptional factors and cytokines of CD4(+) T cells. Proportions of Th1, Th2, Th17, and Treg cells in peripheral blood were detected by flow cytometry. Plasma cytokine concentrations were measured by ELISA. The proportions of Th2 and Th17 cells increased significantly in children with acute HSP (P < 0.05), while there were no significant differences between HSP and healthy controls regarding the proportions of Treg cells and Th1 cells (P > 0.05). mRNA levels of transcriptional factors and cytokines of Th2 and Th17 cells were significantly up-regulated (P < 0.05), while the differences were not significant as to those of Th1 and Treg cells (P > 0.05). Plasma concentrations of IL-17A, IL-4, and IL-6 in patients with HSP were found to be much higher than those of the control group (P < 0.05), and no differences between IFN-γ, IL-12, and TGF-β were detected between the two groups (P > 0.05). Presence of higher proportions of Th2 and Th17 cells in patients with HSP could be closely correlated with aberrant creation of antibody and development of vessel vasculitis. The changes in cytokine milieu in peripheral blood may play an important role in the derangement of CD4(+) T cell subset.

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