Shichishima T, Terasawa T, Hashimoto C, Ohto H, Takahashi M, Shibata A, Maruyama Y
First Department of Internal Medicine, Fukushima Medical College, Japan.
Blood. 1993 Apr 1;81(7):1855-62.
We performed a flow cytometric analysis using monoclonal antibodies to decay accelerating factor (DAF) and CD59/membrane attack complex inhibitory factor (CD59/MACIF) in order to investigate the leukemic cells and erythrocytes from a patient with paroxysmal nocturnal hemoglobinuria (PNH) who developed acute myelocytic leukemia. In May 1990, the leukemic cells comprised 70% of the mononuclear cells in the bone marrow and 76% of those in the peripheral blood. They consisted of a mixture of positive and negative populations, including single DAF-positive cells. In August 1990, almost 100% of the peripheral mononuclear cells were leukemic blasts, and these consisted of a single population with reduced DAF expression. Single-color flow cytometric analysis showed that the leukemic cells lacked CD59/MACIF, while control leukemic cells (n = 3) expressed both DAF and CD59/MACIF. Leukemic blasts from this patient and six control patients expressed lymphocyte function-associated antigen 3 and FcIII receptors (CD 16) both before and after treatment with phosphatidylinositol-specific phospholipase C. The patient's erythrocytes lacking DAF and CD59/MACIF expression corresponded to the proportion of complement-sensitive cells at the onset of acute leukemia. These DAF- and CD59/MACIF-deficient erythrocytes disappeared almost completely with progression of the leukemia. In conclusion, it appears that the expression of glycosylphosphatidylinositol-linked membrane proteins by leukemic cells was heterogeneous and discordant in our patient, and that the leukemic cells were derived from the PNH clone because of their deficiency of CD59/MACIF. It is also suggested that DAF could compete more effectively than CD59/MACIF for a limited number of anchor molecules available on the proliferating leukemic cells.
为了研究一名阵发性夜间血红蛋白尿（PNH）并发急性髓细胞白血病患者的白血病细胞和红细胞，我们使用抗衰变加速因子（DAF）和CD59/膜攻击复合物抑制因子（CD59/MACIF）的单克隆抗体进行了流式细胞术分析。1990年5月，白血病细胞占骨髓单个核细胞的70%，外周血单个核细胞的76%。它们由阳性和阴性群体混合组成，包括单个DAF阳性细胞。1990年8月，几乎100%的外周单个核细胞为白血病原始细胞，这些细胞由DAF表达降低的单一群体组成。单色流式细胞术分析显示，白血病细胞缺乏CD59/MACIF，而对照白血病细胞（n = 3）同时表达DAF和CD59/MACIF。该患者及6名对照患者的白血病原始细胞在磷脂酰肌醇特异性磷脂酶C治疗前后均表达淋巴细胞功能相关抗原3和FcIII受体（CD 16）。患者缺乏DAF和CD59/MACIF表达的红细胞与急性白血病发病时补体敏感细胞的比例相对应。随着白血病的进展，这些缺乏DAF和CD59/MACIF的红细胞几乎完全消失。总之，在我们的患者中，白血病细胞糖基磷脂酰肌醇连接膜蛋白的表达似乎是异质性的且不一致，并且白血病细胞由于缺乏CD59/MACIF而源自PNH克隆。还提示DAF比CD59/MACIF能更有效地竞争增殖白血病细胞上有限数量的锚定分子。
