论文部分内容阅读
以ＨＵＶＥＣ和ＰＡＥＣ为靶细胞，人ＰＢＮＫ和ＮＫ９２为效应细胞，研究了人ＮＫ 细胞对同种和异种内皮细胞杀伤的差异性；并通过酸处理内皮细胞及抗体封闭 ＭＨＣＩ 类分子、ＣＤ９４和ＫＩＲ（ＮＫＢ１），研究了ＭＨＣⅠ类分子对人ＮＫ细胞杀伤ＨＵＶＥＣ和ＰＡＥＣ 的影响．结果表明，ＰＢＮＫ和ＮＫ９２对ＰＡＥＣ的杀伤均大于对ＨＵＶＥＣ的杀伤．酸处理 后，两种ＮＫ细胞对ＨＵＶＥＣ杀伤的增加幅度大于对ＰＡＥＣ的；此外，抗ＣＤ９４单抗未 能改变ＮＫ的杀伤效应；ＫＩＲ（ＮＫＢ１）封闭使ＰＢＮＫ杀伤ＨＵＶＥＣ增加９５％，杀伤ＰＡＥＣ 仅增加 ２９％．以上结果提示： ＮＫ细胞对异种内皮细胞 ＭＨＣⅠ类分子的差异识别作用 可能是ＮＫ细胞杀伤ＰＡＥＣ的主要原因，而ＫＩＲ很可能是ＮＫ杀伤内皮细胞时主要的 传递抑制信号的受体．
Using HUVEC and PAEC as target cells and human PBNK and NK92 as effector cells, the effects of human NK cells on the killing of the same and xenogeneic endothelial cells were studied. The endothelial cells and antibody-blocked MHC class I molecules, CD94 and KIR ( NKB1) to study the effect of MHC class I molecules on human NK cells killing HUVEC and PAEC. The results showed that PBNK and NK92 kill PAEC more than HUVEC. In addition, anti-CD94 mAb failed to change the killer effect of NK; KIR (NKB1) blockade increased PBNK-killing HUVEC by 95% and killing PAEC only increased 29%. The above results suggest that NK cell differentiation of MHC class I molecules in endothelial cells may be the main reason for NK cell killing PAEC, and KIR is likely to be the main killer of endothelial killer delivery inhibitor signal receptor.