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NK细胞杀伤ARH-77细胞的活性及机制的初步探讨
NK细胞杀伤ARH-77细胞的活性及机制的初步探讨
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NK细胞杀伤ARH-77细胞的活性及机制的初步探讨
NK细胞杀伤ARH-77细胞的活性及机制的初步探讨

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NK细胞杀伤ARH-77细胞的活性及机制的初步探讨
NK细胞杀伤ARH-77细胞的活性及机制的初步探讨
Journal Article

NK细胞杀伤ARH-77细胞的活性及机制的初步探讨

2011
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Overview
目的探讨同种异体NK细胞杀伤人骨髓瘤ARH-77细胞的活性及机制。方法 LDH释放法检测NK细胞杀伤ARH-77细胞的活性;RT-PCR方法和流式细胞仪分别检测K562和ARH-77细胞NKG2D配体和HLA-I基因和分子。阻断K562和ARH-77细胞NKG2D配体,观察NK细胞杀伤活性的变化。结果相同效靶比时NK细胞杀伤ARH-77细胞的活性明显低于杀伤K562细胞。两种细胞均表达MICA/B和ULBP1~3基因。K562细胞高表达MICA/B和ULBP1~3分子,不表达HLA-Ⅰ类分子;ARH-77细胞低表达ULBP1~3分子,高表达HLA-Ⅰ类分子。ARH-77细胞HLA基因型为A2、3,B15、35,Cw3、4。阻断NKG2D配体,NK细胞对K562细胞的杀伤活性明显降低,对ARH-77细胞的杀伤活性无明显改变;阻断HLA-Ⅰ类分子后,NK细胞对K562细胞的杀伤活性无变化,对ARH-77细胞的杀伤活性明显提高。结论 ARH-77细胞对NK细胞的杀伤敏感性低,其机制与其高表达HLA-Ⅰ类分子、低表达NKG2D配体有关。
Publisher
河南省肿瘤医院血液科、河南省血液病研究所,河南郑州,450003%南方医科大学珠江医院血液科,广东广州,510282

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