二例重型再生障碍性贫血患者血清体外加速正常人CD34+细胞凋亡的研究

目的：了解再生障碍性贫血患者血清中的造血抑制物及其与造血细胞过度凋亡之间的关系。方法：应用甲基纤维素体外培养法，亲和层析法，ＤＮＡ末端标记及流式细胞术分析观察２例重型再生障碍性贫血Ⅰ型（ＳＡＡⅠ）患者血清在体外抑制正常人骨髓造血祖细胞增殖及促进正常人ＣＤ３４＋细胞凋亡的作用。结果：２例患者血清在体外均可明显抑制正常人ＢＦＵＥ及ＣＦＵＧＭ的增殖，这种抑制活性存在于血清ＩｇＧ片段中，为非补体依赖性。患者血清及ＩｇＧ片段在体外均可加速正常人ＣＤ３４＋细胞凋亡，其中ＩｇＧ较血清的促凋亡作用更为显著（Ｐ均＜０．０１）。经研究证实这种ＩｇＧ可特异性吸附于ＣＤ３４＋细胞表面。经甲泼尼龙治疗后的恢复期血清上述作用消失。结论：某些ＳＡＡⅠ患者血清中存在促进ＣＤ３４＋细胞过度凋亡的造血抑制物ＩｇＧ，造血细胞过度凋亡是患者发病机制之一。甲泼尼龙对这类患者疗效显著

Induction of apoptosis of CD 34 cells by serum from two patients with severe aplastic anemia

Objective:To explore the relationship between the hematopoietic inhibitor and apoptosis of CD 34 cells in patients with severe aplastic anemia (SAA). Methods: The inhibiting activity to the growth of both BFU E and CFU GM was analysed by in vitro methylcellulose culture and CD 34 cell apoptosis was assayed with a kit of programed cell death assay and flow cytometry. Results: Sera from two SAA patients suppressed the growth of normal hematopoietic progenitor cells and induced CD 34 cell apoptosis. Serum immunoglobulin fraction assay showed that the inhibiting activity was in the IgG fraction which bound specifically to CD 34 cells. Conclusion: There was an inhibitive IgG fraction, which induced CD 34 cell apoptosis, in the serum of SAA patients and CD 34 cell apoptosis might be a part of the pathogenesis of SAA.