Significance of the expression of Toll-like receptor and costimulatory molecule of dendritic cells in the peripheral blood in children with Henoch-Sch(o)nlein purpura / 中华实用儿科临床杂志

ABSTRACT

Objective To observe the expression of Toll-like receptor(TLR) on peripheral blood dendritic cells(DC) in children with Henoch-Schtinlein purpura(HSP),and to investigate the pathogenesis of the abnormal expression of TLR in children with HSP.Methods Twenty hospitalized children with HSP in the Affiliated Hospital of Qingdao University Medical College from Dec.2011 to Jul.2012 were enrolled in the study(HSP group).Twenty agemetched healthy children were selected as a healthy control group.Peripheral venous blood was sampled under aseptic condition,peripheral blood mononuclear cells (PBMC) were isolated from density gradient centrifugation,and DC were generated by recombinat human granulocyte-macrophage colony-stimulating factor(GM-CSF),interleukin-4(IL-4) and tumor necrosis factor-α(TNF-α) in vitro.Expressions of CD83,CD86 and TLR2,TLR3,TLR4 in peripheral blood DC were examined by fluorescent activated cell sorter (FACS).Results 1.No significant distinction was found in the expression of the C Ds3 on peripheral blood DC between HSP group and healthy control group(t =0.80,P ＞ 0.05) ;in HSP group had remarkably increased expression of the CD86 on peripheral blood DC than that of the healthy control group (t =9.56,P ＜ 0.01).2.Expression rates of TLR2,TLR3,TLR4 on peripheral blood DC in the HSP group were higher than those in the healthy control group(t =1 1.79,13.29,9.45,all P ＜ 0.01).3.Expression rates of TLR2,TLR3 and TLR4 in HSP group had positive correlation with expression rates of CD86 (r =0.84,P ＜ 0.01 ; r =0.53,P ＜ 0.05 ; r =0.66,P ＜ 0.05).Conclusions Expressions of TLR2,TLR3 and TLR4 on peripheral blood DC significantly increased and were positively correlated with expression of CD86.This implies that TLR and co-stimulatory molecules might participate in the pathogenesis of HSP by mediating signal transduction,leading to abnormity of cytokines,then inducing Th1/Th2 immune imbalance by showing the advantage of Th2 function.