Wei Hui, Tian Zheng, Wang Xiao-Jing, Liu Kai-Qi, Zhang Cui-Ping, Wang Hui-Jun, Mi Ying-Chang, Wang Jian-Xiang
Institute of Hematology & Blood Disease Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300020, China.
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2010 Oct;18(5):1105-8.
CD59 is a glycosyl-phosphatidyl inositol-anchored protein with the capacity to block the formation of membrane-attack complex, and protect the cells from complement-mediated cytolysis. The study was aimed to investigate whether CD59 is deficient in acute promyelocytic leukemia (APL) blast cells. Expression of CD59 on APL blast cells was analysed by flow cytometry. Expression of CD59 on NB4 cells was determined by flow cytometry before and after treating with all trans retinoic acid (ATRA). Pig-A gene coding region was sequenced. The results showed that the deficiency of CD59 expression in 12 out of 19 APL samples was found, its incidence was significantly higher than that in other acute myeloid leukemia (AML) samples (deficiency of CD59 expression in 14 of 40 non-APL AML samples, p=0.042). The expression of CD59 became normal after the patients achieved complete remission (CR), which indicated that the deficient of CD59 expression was only found in APL blast cells, but also found in APL cell line NB4 cells. The expression of CD59 was not changed after NB4 cells were induced to differentiate by ATRA. Sequencing pig-A gene coding region of NB4 cells and one APL patient with deficiency of CD59 displayed that the mutation of pig-A gene was not observed, therefore the deficiency of CD59 expression in APL cells did not result from mutation of pig-A gene. It is concluded that the deficiency of CD59 expression exists in APL blast cells more probably.
CD59是一种糖基磷脂酰肌醇锚定蛋白,具有阻止膜攻击复合物形成的能力,并保护细胞免受补体介导的细胞溶解作用。本研究旨在调查急性早幼粒细胞白血病(APL)原始细胞中CD59是否缺乏。采用流式细胞术分析APL原始细胞上CD59的表达。用全反式维甲酸(ATRA)处理前后,通过流式细胞术测定NB4细胞上CD59的表达。对Pig-A基因编码区进行测序。结果显示,19例APL样本中有12例存在CD59表达缺陷,其发生率显著高于其他急性髓系白血病(AML)样本(40例非APL AML样本中有14例存在CD59表达缺陷,p = 0.042)。患者达到完全缓解(CR)后,CD59表达恢复正常,这表明CD59表达缺陷不仅见于APL原始细胞,也见于APL细胞系NB4细胞。NB4细胞经ATRA诱导分化后,CD59表达未发生变化。对NB4细胞及1例CD59缺陷的APL患者的Pig-A基因编码区进行测序,结果显示未观察到Pig-A基因突变,因此APL细胞中CD59表达缺陷并非由Pig-A基因突变所致。结论是,APL原始细胞中更可能存在CD59表达缺陷。