| Objective To investigate the function of Th17 cells and change of CD4+CD25+ T regulatory (Treg) cells in children with Henoch-Schonlein purpura (HSP) in acute and explore their roles in immunological pathogenesis of HSP.Methods Thirty healthy children were recruited as control. Fifty-four patients with HSP were involved in this study, who were randomized into Henoch-Schonlein-Purpura-Nephritis(HSPN) group and non-HSPN(NHSPN) group based on the urine analysis results. The plasma level of IL-17 was measured by ELISA. Flow cytometric analysis (FCM) was performed to detect the percentage of CD4+CD25+Treg cells,CD4+cells and CD8+cells, CD4+/CD8+ratio, and the levels of CD3+ cells,NK cells(CD3-CD56+),B cells (CD19+) and CD3+HLADR+ cells in peripheral blood.Results①Compared with healthy control subjects(29.75±21.65)ng/L, plasma level of IL-17 was significantly up-regulated during the acute phase of HSP(86.65±13.90ng/L,t=14.66,P<0.01). There was no significant difference between HSP group and NHSPN group (q=2.136,P>0.05).②Compared with healthy control subjects (3.93±0.42) %, the proportions of CD4+CD25+Treg cells in peripheral blood were significantly lower than that in patients with HSP (2.25±1.02%,t=7.28,P<0.01). No significant difference was found between HSP group and NHSPN group (q=3.703,P>0.05). CD4+CD25+ Treg cells in the children with HSP was positively correlated with CD4+ cells, CD4+/CD8+ ratio,respectively (r=0.554,0.506,P<0.01), and was negatively correlated with CD19+cells(r=-0.305, P<0.05), but had no correlation with CD8+. CD3+, CD3-CD56+ and CD3+HLADR+ cells(r=-0.093,0.287,0.082,-0.109, P>0.05).③Plasma level of IL-17 in the children with HSP was negatively correlated with CD4+CD25+Treg cells (r=-2.95,P<0.05)Conclusions①Increase plasma level of IL-17 and enhanced Th17 cell function were found in children with acute HSP.②The level of CD4+CD25+Treg cells in peripheral blood in children with acute HSP decreased, indicating inhibited immune regulative role.③The imbalance of Th17/Treg existed in children with HSP and that involved in the pathogenesis of HSP. |