NKG2D-MICA/B在急性白血病免疫逃逸机制中的作用

目的探讨NK细胞活化性受体（NKG2D）-MICA/B在急性白血病肿瘤免疫逃逸机制中的作用。方法选择20例初发未治疗的急性白血病患者,应用流式细胞术检测白血病细胞表面MICA/B表达水平、ELISA法检测血清可溶性MICA及MICB（sMICA,sMICB）水平,同时检测患者NKG2D表达水平。选择5例健康人做为对照。结果（1）20例急性白血病患者白血病细胞表面不表达或弱表达MICA/B,正常人淋巴细胞表面不表达MICA/B。（2）患者血清sMICA和sMICB水平均高于对照组,差异有统计学意义（P〈0.01）。（3）患者NKG2D表达水平低于对照组,差异有统计学意义（P〈0.01）。结论白血病细胞表面MICA和MICB的脱落损伤基于NKG2D-MIC的抗白血病效应,可能是导致急性白血病免疫逃逸的机制之一。

Primary Study on the Immune Evasion Mechanism In Acute Leukemia Mediated by the Active Receptor of NK Cell NKG2D and the Ligand MICA/B

Objective To analyze the immune escaping based on NK cell receptor NKG2D-MIC interaction in acute leukemia. Methods Twenty untreated patients and five healthy donors were studied. The flow cytometry analysis was used to detect the NKG2D and its ligand MICA/B in the peripheral blood of the patients and the donors, ELISA was used to detect the levels of soluble MICA and MICB（sMICA, sMICB） in the sera. Results （1）MICA/B were not expressed or at very low levels on leukemia cells of the patients. Of the healthy donors, there was not MICA/B expression on lymphocyte. （2） Sera of patients, but not of healthy donors, contained elevated levels of sMICA and sMICB （P〈0.01）. The expression of NKG2D on NK cells in patients was lower than that on the donors （P〈0. 01）. Conclusions Reduction of leukemia MIC surface expression by shedding may impair NKG2D-mediated anti-leukemia effect and lead to the immune escaping of acute leukemia.