在穿孔素缺陷小鼠中，由T细胞和自然杀伤细胞介导的细胞毒性会大大受损。
Cytotoxicity mediated by T cells and natural killer cells is greatly impaired in perforin-deficient mice.
作者信息
Kägi D, Ledermann B, Bürki K, Seiler P, Odermatt B, Olsen K J, Podack E R, Zinkernagel R M, Hengartner H
机构信息
Department of Pathology, University of Zürich, Switzerland.
出版信息
Nature. 1994 May 5;369(6475):31-7. doi: 10.1038/369031a0.
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.
通过同源重组产生了穿孔素缺陷型小鼠，以确定CD8 + 细胞毒性T细胞和自然杀伤细胞的作用是否由涉及穿孔素的孔形成介导。这些小鼠存活且可育，CD8 + T细胞和自然杀伤细胞数量正常，它们在体外不会裂解病毒感染的或同种异体成纤维细胞或自然杀伤靶细胞。这些小鼠无法清除淋巴细胞性脉络丛脑膜炎病毒，并且它们清除纤维肉瘤肿瘤细胞的效率降低。因此，穿孔素是T细胞和自然杀伤细胞介导的细胞溶解的关键效应分子。
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