目的 通过研究细胞因子信号转导抑制因子（SOCS）低甲基化与过敏性紫癜（HSP）患儿Th17/Treg细胞失衡的关系，探讨HSP的免疫发病机制。方法 选取2014年5月至2015年1月32例急性期HSP住院患儿为研究对象，另选取行健康体检的28例儿童作为健康对照组。采用ELISA法检测血浆IL-6水平；流式细胞术检测外周血CD4⁺IL-17A⁺T细胞（Th17细胞）比例、CD4⁺CD25⁺调节性T细胞（Treg）比例和CD4⁺T细胞磷酸化STAT3（pSTAT3）蛋白平均荧光强度（MFI）；实时荧光定量PCR（RT-qPCR）技术检测CD4⁺T细胞SOCS1、SOCS3基因mRNA表达；高分辨率熔解曲线（HRM）分析法检测外周血单个核细胞SOCS1基因外显子2、SOCS3基因5'端非翻译区（5'-UTR）可能的STAT3结合位点CpG岛甲基化水平。结果 与健康对照组比较，HSP组血浆IL-6浓度、CD4⁺T细胞pSTAT3的MFI显著增加；HSP组Th17细胞比例显著上调，Treg细胞比例显著下调（P < 0.05）。HSP组患儿急性期外周血单个核细胞SOCS1 mRNA和SOCS3 mRNA水平均显著高于健康对照组（P < 0.05）；HSP组SOCS1 mRNA及SOCS3 mRNA表达均与Th17/Treg比值呈负相关（P < 0.05）。HSP组患儿急性期SOCS1基因外显子2、SOCS3基因5'-UTR区可能的STAT结合位点CpG岛呈低甲基化，而健康对照组呈完全去甲基化状态。结论 SOCS1、SOCS3基因低甲基化所致其相对表达不足可能是HSP患儿Th17/Treg失衡的因素之一。

Objective To investigate the association between suppressor of cytokine signaling (SOCS) hypomethylation and T helper 17 (Th17) cell/regulatory T (Treg) cell imbalance in children with Henoch-Schönlein purpura (HSP) and the immune pathogenesis of HSP. Methods A total of 32 children in the acute stage of HSP who were hospitalized from May 2014 to January 2015 were enrolled as subjects, and 28 children who underwent physical examination were enrolled as normal control group. ELISA was used to measure the plasma level of interleukin-6 (IL-6). Flow cytometry was used to measure the percentages of CD4⁺ IL-17A⁺ T cells (Th17 cells) and CD4⁺CD25⁺ Treg cells (Treg cells) in peripheral blood and mean fluorescence intensity (MFI) for phosphorylated-STAT3 (pSTAT3) protein in CD4⁺ T cells. Quantitative real-time PCR was used to measure the mRNA expression of suppressor of cytokine signaling-1 (SOCS1) and suppressor of cytokine signaling-3 (SOCS3) in CD4⁺ T cells. High-resolution melting (HRM) was used to evaluate the methylation level of the CpG islands in SOCS1 exon 2 and the CpG islands of the potential bind sites for STAT3 in the 5'-untranslated region (5'-UTR) of SOCS3 in peripheral blood mononucleated cells. Results Compared with the normal control group, the HSP group had significant increases in plasma IL-6 concentration and MFI for pSTAT3 in CD4⁺ T cells, as well as a significant increase in the percentage of Th17 cells and a significant reduction in the percentage of Treg cells (P < 0.05). The HSP group had significantly higher mRNA expression of SOCS1 and SOCS3 in peripheral blood mononucleated cells than the normal control group (P < 0.05). In the HSP group, the mRNA expression of SOCS1 and SOCS3 was negatively correlated with Th17/Treg ratio (P < 0.05). The HSP group had hypomethylation of the CpG islands in SOCS1 exon 2 and the potential binding site for STAT3 in SOCS3 5'-UTR, while the normal control group had complete demethylation. Conclusions Low relative expression of SOCS1 and SOCS3 caused by hypomethylation may be a factor for Th17/Treg imbalance in children with HSP.