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目的:研究CD226在再生障碍性贫血(简称再障,AA)患者外周血T淋巴细胞亚群上的表达率及其与血清中IL-2、IFN-γ、IL-4、IL-10浓度的关系,以探讨其在AA发病机制中的作用。方法:60例AA患者和30例正常对照者外周血单个核细胞,四色荧光标记的单克隆抗体染色,利用流式细胞仪测定T淋巴细胞亚群上CD226的表达率;用ELISA法检测血清中IL-2、IFN-γ、IL-4、IL-10的浓度。结果:重型再障(SAA)和非重型再障(NSAA)患者CD3+、CD3+CD4+和CD3+CD8+T淋巴细胞上CD226的表达率与正常对照组相比均差异有统计学意义(均P<0.05),尤其SAA患者CD3+、CD3+CD8+T淋巴细胞上CD226表达率显著性高于正常对照组(P<0.01),而SAA与NSAA之间差异无统计学意义。SAA和NSAA患者血清中IL-2、IFN-γ水平与正常对照组相比差异有统计学意义(P<0.05);IL-4、IL-10水平与正常对照组相比差异有统计学意义(P<0.01)。AA患者CD3+T淋巴细胞上CD226表达率与血清中IL-2、IFN-γ水平呈正相关(r值分别为0.129、0.200);与IL-4、IL-10水平呈负相关(r值分别为-0.095、-0.147)。结论:AA的发病不仅与T细胞功能紊乱及其分泌的Th1型细胞因子增高有关,还与Th2型细胞因子相对不足有关。AA患者T淋巴细胞的异常活化需要CD226的参与,CD226异常高表达可能与AA的免疫发病有关。
Objective: To investigate the expression of CD226 in peripheral blood T lymphocyte subsets of patients with aplastic anemia (AA) and its relationship with the serum levels of IL-2, IFN-γ, IL-4 and IL-10 Relationship to explore its role in the pathogenesis of AA. Methods: Peripheral blood mononuclear cells (PBMCs) from 60 patients with AA and 30 normal controls were stained with four-color fluorescently labeled monoclonal antibodies. The expression of CD226 on T lymphocyte subsets was determined by flow cytometry. Serum IL-2, IFN- [gamma], IL-4, IL-10 concentrations. Results: The expression rates of CD226 on CD3 +, CD3 +, CD4 + and CD3 + CD8 + T lymphocytes in patients with severe aplastic anemia (SAA) and non-severe aplastic anemia (NSAA) were significantly different from those in normal control group <0.05). In particular, the expression of CD226 on CD3 + and CD3 + CD8 + T lymphocytes in SAA patients was significantly higher than that in normal controls (P <0.01), but there was no significant difference between SAA and NSAA. The levels of IL-2 and IFN-γ in serum of patients with SAA and NSAA were significantly lower than those in normal control group (P <0.05). The levels of IL-4 and IL-10 in patients with SAA and NSAA were significantly lower than those in normal control (P <0.01). The expression of CD226 on CD3 + T lymphocytes in patients with AA was positively correlated with the levels of IL-2 and IFN-γ in serum (r = 0.129,0.200, respectively), and negatively correlated with the levels of IL-4 and IL-10 -0.095, -0.147). Conclusion: The pathogenesis of AA is not only related to the disorder of T cells and the increased secretion of Th1 cytokines, but also to the relative deficiency of Th2 cytokines. Abnormal activation of T lymphocytes in patients with AA requires the involvement of CD226, abnormal expression of CD226 may be related to the AA immune pathogenesis.