过敏性紫癜患儿外周血CD4^+记忆T细胞亚群表达的意义

Clinical significance of CD4^+ memory T cell subsets in the patients with Henoch-Schonlein purpura

目的探讨CD4+记忆T细胞亚群在过敏性紫癜(HSP)免疫发病机制中的意义。方法收集初发HSP患儿25例,并将其分为HSP无肾脏损害组(N-HSPN组)15例和紫癜性肾炎组(HSPN组)10例,另选取10例本院健康体检儿童作为正常对照组,抽取患儿急性期、恢复期外周血,用梯度密度离心法分离新鲜单个核细胞(PBMC),用流式细胞仪检测PBMC中CD4+效应记忆T细胞(CD4+Tem)、CD4+中央记忆T细胞(CD4+Tcm)水平。结果 HSP患儿急性期外周血CD4+T细胞水平、CD4+/CD8+比例均较正常组降低(均<0.05),而CD8+T细胞数水平与正常组比较差异无统计学意义(>0.05)。急性期N-HSPN和HSPN组患儿外周血CD4+Tem水平均明显高于正常对照组(均<0.05),而N-HSPN和HSPN组比较差异无统计学意义(>0.05);N-HSPN和HSPN患儿CD4+Tcm的表达与正常组比较差异均无统计学意义(均>0.05)。恢复期NHSPN和HSPN组HSP患儿外周血CD4+Tem水平仍明显升高,与急性期比较差异无统计学意义(均>0.05),但仍然明显高于正常组(均<0.05)。结论 HSP患儿存在CD4+T细胞的异常,CD4+Tem的异常升高可能是HSP发生的一个重要因素;CD4+Tem可能只是参与了HSP血管炎的免疫损伤,而与是否导致HSPN的病理过程无关,不能作为检测HSP肾脏损害的有效指标。

Objective To explore the significance of CD4^＋Tmcell subsets in the immunopathogenesis of the Hen-och-Schonlein purpura （HSP）. Methods Twenty-five patients with HSP who were hospitalized for the first time were divided into N-HSPN group （15 cases） and HSPN group （ten cases）, and another ten health children were selected as health control group. Fresh peripheral blood mononuclear cells （PBMC） from vein at acute and convalescent phases were isolated by density gradient centrifugation. The level of CD4^＋Tem cell, CD4^＋Tcm cell on PBMC was analyzed by flow cytometry. Results Compared with the healthy control group, the level of CD4^＋T cell and the ratio of CD4^＋/CD8^＋ were both lower （P 〈 0.05） in HSP group at the acute phase; Whereas there was no significant difference of the level of CD8^＋T cell between the HSP group and healthy control group （P 〉 0.05）.The level of CD4^＋ Tern cell were both significantly higher in N-HSPN and HSPN group during the acute phase than that in healthy control group（P 〈 0.01 ）. There was no significant difference of the level of CD4^＋Tem cell between the N-HSPN group and HSPN group （P 〉 0.05）. There was also no significant difference of the level of CD4^＋Tcm cell betweenN-HSPN and HSPN group and healthy control group（P 〉 0.05） .There was no significant difference of the level of CD4^＋ Tem-cell in N-HSPN and HSPN group between the acute phase and the convalescent phase（P 〉 0.05）, and it was still higher than that in the healthy control group （P 〈 0.01）. Conclusions The high lever of CD4^＋Tem cell may be as a reason of the accidence of liSP. CD4^＋Tem cells maybe only participate the immunopathogenesis of liSP, and have nothing to do with the pathogenesis of HSPN, and it can not serve as an effective marker of renal injury in children with HSP.