CYTOTOXICITY MEDIATED BY T-CELLS AND NATURAL-KILLER-CELLS IS GREATLY IMPAIRED IN PERFORIN DEFICIENT MICE
CYTOTOXICITY MEDIATED BY T-CELLS AND NATURAL-KILLER-CELLS IS GREATLY IMPAIRED IN PERFORIN DEFICIENT MICE
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DOI：
10.1038/369031a0
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发表时间：
1994-05-05
期刊：
影响因子：
64.8
通讯作者：
HENGARTNER, H
中科院分区：
文献类型：
--
作者：
KAGI, D;LEDERMANN, B;HENGARTNER, H
通过同源重组产生穿孔蛋白缺陷小鼠，以确定CD8（+）细胞溶解性T细胞和自然杀伤细胞的作用是否由涉及穿孔蛋白的孔形成介导。这些小鼠是活的和可生育的，并且具有正常数量的CD8（+）T细胞和自然杀伤细胞，其在体外不裂解病毒感染的或同种异体的成纤维细胞或自然杀伤靶细胞。小鼠不能清除淋巴细胞性脉络丛脑膜炎病毒，并且它们消除纤维肉瘤肿瘤细胞的效率降低。因此，穿孔蛋白是T细胞和天然巨噬细胞介导的细胞溶解的关键效应分子。
Perforin-deficient mice have been generated by homologous recombination to determine whether the effects of CD8(+) cytolytic T cells and natural killer cells are mediated by pore formation involving perforin. These mice are viable and fertile and have normal numbers of CD8(+) T cells and natural killer cells which do not lyse virus-infected or allogeneic fibroblasts or natural killer target cells in vitro. The mice fail to clear lymphocytic choriomeningitis virus and they eliminate fibrosarcoma tumour cells with reduced efficiency. Perforin is therefore a key effector molecule for T-cell- and natural killer-cell-mediated cytolysis.