Fang Xin-Chen, Liu Hui-Lan, Sun Zi-Min, Gui Li, Geng Liang-Quan, Wang Xing-Bin, Zhou Miao, Wang Zu-Yi
Graduate school, Anhui Medical University, and Department of Hematology, Provincial Hospital, Hefei 230001, Anhui Province, China.
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2010 Apr;18(2):436-40.
This study was aimed to explore the immune escaping mechanisms based on expression and abscission of human natural killer (NK) cell activating receptors NKG2D and their ligands MICA/B, ULBP-1, 2, 3 in patients with acute leukemia (AL). 30 de novo AL patients and 10 healthy persons (control) were enrolled in study. Flow cytometry was used to detect the expression levels of MICA/B, ULBP-1, 2, 3 on leukemic cells. ELISA was used to detect the levels of soluble MICA (sMICA), solube MICB (sMICB) and soluble ULBP-1, -2, -3 in the serum. The results showed that sMICA, sMICB and ULBP-1, -2, -3 were not expressed or expressed at very low levels on leukemia cells of the patients; the levels of free sMICA and sMICB in serum of AL patients were higher than that in serum of healthy persons, there was significant difference (p<0.01). But the levels of ULBP 1-3 in serum of AL patients did not show obvious statistical difference as compared with healthy persons (p>0.05). It is concluded that the negative or low expression of NKG2D ligands (MICA, MICB and ULBPs) on surface of acute leukemia cells may lead to the immune escape of leukemia cells, the abscission of MICA and MICB, and the deficiency of ULBP expression on leukemia cells may be one of immune escape mechanisms of leukemia cells.
本研究旨在探讨急性白血病（AL）患者基于人类自然杀伤（NK）细胞活化受体NKG2D及其配体MICA/B、ULBP-1、2、3的表达及脱落的免疫逃逸机制。30例初发AL患者和10名健康人（对照组）纳入研究。采用流式细胞术检测白血病细胞上MICA/B、ULBP-1、2、3的表达水平。采用酶联免疫吸附测定（ELISA）检测血清中可溶性MICA（sMICA）、可溶性MICB（sMICB）及可溶性ULBP-1、-2、-3的水平。结果显示，患者白血病细胞上sMICA、sMICB及ULBP-1、-2、-3不表达或表达水平极低；AL患者血清中游离sMICA和sMICB水平高于健康人血清，差异有统计学意义（p<0.01）。但AL患者血清中ULBP 1-3水平与健康人相比无明显统计学差异（p>0.05）。结论：急性白血病细胞表面NKG2D配体（MICA、MICB和ULBPs）的阴性或低表达可能导致白血病细胞免疫逃逸，MICA和MICB的脱落以及白血病细胞上ULBP表达缺陷可能是白血病细胞免疫逃逸机制之一。
