【摘要】 目的:探讨获得性再生障碍性贫血(AA)患者T细胞表面VLA-4、CX3CR1的表达在AA发病机制中的作用。方法:①流式细胞术分析46例AA患者(20例重型AA,26例非重型AA)骨髓和外周血中T淋巴细胞亚群的变化以及VLA-4、CX3CR1在T淋巴细胞亚群上的表达。②ELISA方法测定其骨髓和外周血浆中VCAM-1(VLA-4的配体)、Fractalkine(CX3CR1的配体)的含量。结果:①AA患者外周血中CD3+细胞比例基本正常(P>0.05),CD8+细胞比例明显上升,CD4+细胞比例明显下降(P<0.01);骨髓中CD3+、CD8+细胞比例均明显升高(P<0.01),CD4+细胞比例减低仅在重型AA患者中差异有统计学意义(P<0.05)。②AA患者骨髓和外周血T细胞亚群表面VLA-4的表达与对照组比较均差异无统计学意义(均P>0.05)。然而患者骨髓和外周血中CD3+/CX3CR1+细胞、CD3+/CD4+/CX3CR1+细胞以及CD3+/CD8+/CX3CR1+细胞比例均升高(P<0.05),尤其CD3+/CD8+/CX3CR1+细胞比例升高更为显著(P<0.01)。③AA患者骨髓和外周血浆中VCAM-1水平与对照组比较均无明显变化(P>0.05)。而Fractalkine水平在重型和非重型AA患者骨髓中以及重型AA患者外周血浆中均升高(P<0.05)。结论:获得性AA作为一种T细胞介导的免疫性疾病,存在T细胞亚群失衡。T细胞通过高表达CX3CR1,与Fractalkine相互作用,从外周血迁移到骨髓,并在骨髓中积聚导致造血干/祖细胞的破坏。更多还原

【Abstract】 Objective:To investigate the contribution of the expression of VLA-4 and CX3CR1 on T cells surface to the pathogenesis of acquired aplastic anemia (AA).Method:①The percentage of T cell subsets and the expression of VLA-4 and CX3CR1 on T cells from peripheral blood and bone marrow were analyzed by flow cytometry in 46 AA patients (20 with severe aplastic anemia and 26 with non-severe aplastic anemia). ②The levels of VCAM-1 (ligand of VLA-4) and Fractalkine (ligand of CX3CR1) were investigated in blood and bone marrow from AA patients and controls by Enzyme-linked immunosorbent assay.Result:①In peripheral blood,there was no significant difference of the percentage of CD3+ cells (P>0.05). But increased CD8+ cells and reduced CD4+ cells were found in AA patients (P<0.01). In bone marrow,both the percentage of CD3+ cells and CD8+ cells were increased in AA patients (P<0.01). And significantly lower percentage of CD4+ cells was only found in SAA patients (P<0.05). ②Both in blood and bone marrow,there was no statistically significant difference of the expression of VLA-4 on T cell subsets (P>0.05). However,the percentage of CD3+/CX3CR1+ cells、CD3+/CD4+/CX3CR1+ cells,and especially CD3+/CD8+/CX3CR1+ cells were increased in AA patients compared with controls (P<0.05). ③ There were no significant difference of the levels of VCAM-1 in blood or bone marrow plasma between AA patients and controls (P>0.05),but the plasma levels of Fractalkine were significantly higher in SAA patients’ blood and all the patients’ bone marrow (P<0.05).Conclusion:Acquired AA is a T-cell-media-ted immune disease,and presents abnormal T cell subsets. T cells appear to relocate from peripheral blood and accumulate in bone marrow to destruct hematopoietic stem and progenitor cells,probably due to elevated expression of surface CX3CR1 interacting with Fractalkine.更多还原