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-Schönlein purpura

摘要:

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（r_s=0.615，P < 0.05），与IL-17水平呈负相关（r_s=-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。

Abstract:

Objective To study the role of gamma-delta T (γδ T) cells and its subsets in the immunopathogenesis of Henoch-Schönlein 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 (r_s=0.615, P < 0.05) and was negatively correlated with IL-17 level (r_s=-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.