再生障碍性贫血患者造血祖细胞及免疫机制的研究

目的探讨再生障碍性贫血(再障)的发病机制。方法采用甲基纤维素及胶原半固体培养法对56例再障骨髓CFU-GM、CFU-E、BFU-E及CFU-M K、BFU-M K进行培养;采用APAAP法及双抗体夹心酶联免疫吸附法(EL ISA)对再障患者外周血T细胞亚群、血清sIL-2R进行检测。结果再障患者CFU-GM、CFU-E、BFU-E及CFU-M K、BFU-M K集落数均低于对照组,且严重型再障集落数减少程度与慢性再障相近;再障患者CD 3亚群细胞无变化,CD 4亚群细胞减低,CD 8亚群细胞增高,CD 4/CD 8降低,重型再障患者血清sIL-2R中水平高于正常对照组与慢性再障。结论骨髓造血祖细胞数量减少是再障发病的重要因素,其减少程度与再障的病情有关;细胞免疫功能异常及造血负调控因子可能在再障发病中起一定的作用。

Significance.and detection of hematopoietic progenitor, T lymphocyte subsets and Sil-2R level in patients with aplastic anemia

To explore the pathogenesis of aplastic anemia(AA).Methods CFU-GM,CFU-E,and BFU-E of bone marrows from 56 patients with AA were assayed with methyclluiose semisolid culture method;CFU-MK and BFU-MK of bone marrow were assayed with collagen semisolid culture;T lymphocyte subsets in the peripheral blood mononuclear cells and the levels of sIL2R in the serum in 56 AA patients were measured by APAAP and ELISA respectively. Results The colonies of CFU-GM,CFU-E,BFU-E and CFU-MK,BFU-MK of patients with AA were less than those of the controls.CD3 cells had not changed,CD4 cells and CD4/CD8 cells were lower,and CD8 cells and sIL-2R levels were higher in AA patients than in normal controls.Conclusion The decrease of bone marrow hematopoietic progenitor cells plays important roles in the pathogenesis of AA,and is associated with clinical features.The cellular immune dysfunction and inhibitory hematopoietic cytokines may have a potential role in pathogenesis of AA.