Mombaerts P, Mizoguchi E, Ljunggren H G, Iacomini J, Ishikawa H, Wang L, Grusby M J, Glimcher L H, Winn H J, Bhan A K
Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.
Int Immunol. 1994 Jul;6(7):1061-70. doi: 10.1093/intimm/6.7.1061.
We describe the development and function of the peripheral lymphoid system of mutant mice rendered deficient in either alpha beta or gamma delta T cells via targeting of TCR genes in embryonic stem cells. In the spleen of alpha beta T cell-deficient mice, gamma delta T cells do not compensate in numbers for the lack of alpha beta T cells, but B cells do. alpha beta T cell-deficient mice are unable to mount an antibody response to ovalbumin and do not reject skin allografts. Natural killer cell function is not impaired in any of the mutant mice. TCR mutant mice will prove useful in dissecting differential functions of alpha beta and gamma delta T cells in vivo.
我们描述了通过靶向胚胎干细胞中的TCR基因使αβ或γδ T细胞缺陷的突变小鼠外周淋巴系统的发育和功能。在αβ T细胞缺陷小鼠的脾脏中，γδ T细胞在数量上不能补偿αβ T细胞的缺失，但B细胞可以。αβ T细胞缺陷小鼠无法对卵清蛋白产生抗体反应，也不能排斥皮肤同种异体移植。在任何突变小鼠中，自然杀伤细胞功能均未受损。TCR突变小鼠将有助于在体内剖析αβ和γδ T细胞的不同功能。
