NORMAL DEVELOPMENT OF MICE DEFICIENT IN BETA-2-M, MHC CLASS I PROTEINS, AND CD8+ T-CELLS
NORMAL DEVELOPMENT OF MICE DEFICIENT IN BETA-2-M, MHC CLASS I PROTEINS, AND CD8+ T-CELLS
复制标题
DOI：
10.1126/science.2112266
复制
发表时间：
1990-06-08
期刊：
影响因子：
56.9
通讯作者：
SMITHIES, O
中科院分区：
文献类型：
--
作者：
KOLLER, BH;MARRACK, P;SMITHIES, O
主要组织相容性 I 类蛋白向潜在反应细胞展示病毒和自身抗原，对 T 细胞的成熟很重要； β2-微球蛋白（β2M）是其正常表达所必需的。源自具有破坏的β2M基因的胚胎干细胞的小鼠嵌合体将失活的基因传递给它们的后代。在进一步育种后，以预期的频率获得了突变的β2M基因纯合的动物。纯合子看起来很正常，尽管在它们的细胞上没有检测到 I 类抗原，而且动物严重缺乏 CD4-CD8+T 细胞，而 CD4-CD8+T 细胞通常介导细胞毒性 T 细胞功能。
Major histocompatibility class I proteins display viral and self antigens to potentially responsive cells and are important for the maturation of T cells; .beta.2-microglobulin (.beta.2M) is required for their normal expression. Mouse chimeras derived from embryonic stem cells with a disrupted .beta.2M gene transmitted the inactivated gene to their progeny. Animals homozygous for the mutated .beta.2M gene were obtained at expected frequencies after further breeding. The homozygotes appeared normal, although no class I antigens could be detected on their cells and the animals are grossly deficient in CD4-CD8+T cells, which normally mediate cytotoxic T cell function.