γδ T细胞在儿童过敏性紫癜免疫微环境中的表达和意义

Expression of gamma-delta T cells in immune microenvironment in children with Henoch-Sch?nlein purpura

目的探讨γδ T细胞及其细胞亚群在儿童过敏性紫癜(HSP)免疫发病机制中的作用,从调控γδ T细胞作为切入点,为儿童HSP的治疗提供新思路。方法以33例HSP患儿(HSP组)和21例健康儿童(健康对照组)为研究对象,比较两组外周血单个核细胞(PBMCs)中γδ T及其细胞亚群Vδ1^+T、Vδ2^+T等表达水平、γδ T细胞凋亡率及IL-17水平。结果 HSP组PBMCs中淋巴细胞比例、γδ T细胞中Vδ2^+T比例低于健康对照组(P < 0.05)。HSP组γδ T细胞中Vδ1^+T比例、血浆IL-17水平高于健康对照组(P < 0.05)。HSP组γδ T细胞总凋亡率低于健康对照组(P < 0.05),其中以早期凋亡为著。Vδ2^+T表达与γδ T细胞总凋亡率呈正相关(rs=0.615,P < 0.05),与IL-17水平呈负相关(rs=-0.398,P < 0.05)。结论γδ T细胞介导的Vδ1+/Vδ2^+T免疫失衡及IL-17炎症因子过度激活可能参与HSP的发生,其中Vδ2^+T诱导的免疫耐受被打破可能是疾病发生的重要病理生理基础。

Objective To study the role of gamma-delta T (γδ T) cells and its subsets in the immunopathogenesis of Henoch-Schonlein purpura (HSP) in children, and to provide new ideas for the treatment of HSP in children from the aspect of γδ T cell regulation.Methods A total of 33 children with HSP were enrolled as the HSP group, and 21 healthy children were enrolled as the healthy control group. The percentages of γδ T cells and its subsets Vδ1^+T and Vδ2^+T cells among peripheral blood mononuclear cells (PBMCs) were measured, as well as the apoptosis rate of γδ T cell and plasma level of interleukin-17 (IL-17).Results Compared with the healthy control group, the HSP group had significantly lower percentages of lymphocytes in PBMCs and Vδ2^+T cells in γδ T cells (P < 0.05). The HSP group had significantly higher percentage of Vδ1^+T cells in γδ T cells and plasma level of IL-17 than the healthy control group. The HSP group had a significantly higher overall apoptosis rate of γδ T cells than the healthy control group (P < 0.05), especially early apoptosis. The percentage of Vδ2^+T cells was positively correlated with overall apoptosis rate (rs=0.615, P < 0.05) and was negatively correlated with IL-17 level (rs=-0.398, P < 0.05).Conclusions Vδ1^+/Vδ2^+T cell immune imbalance mediated by γδ T cells and over-activation of IL-17 may be involved in the development of HSP, among which the disturbance of immune tolerance induced by Vδ2^+T cells plays an important role in the pathophysiology of the disease.