Lauzon R J, Siminovitch K A, Fulop G M, Phillips R A, Roder J C
J Exp Med. 1986 Nov 1;164(5):1797-802. doi: 10.1084/jem.164.5.1797.
Mice with severe combined immunodeficiency syndrome (SCID) exhibit an impairment in both T and B cell maturation, whereas myelopoiesis remains unaffected. We report here that spleens from SCID mice have undergone phenotypic expansion of cells bearing the NK-2 and asialo GM1 markers (70-80%) characteristic of NK cells and this expansion is accompanied by a 3-4-fold enrichment in NK cytolytic activity over their normal C.B-17 littermates. Furthermore, the NK cells from SCID mice do not rearrange or express T cell receptor alpha or beta genes, or a third T cell rearranging gene, gamma. These findings suggest that (a) T cell receptors are not necessary for NK-mediated cytolysis, and (b) either NK cells constitute an entirely distinct lineage or NK cell function is acquired in pre-T cells prior to the expression of T cell receptor genes.
患有严重联合免疫缺陷综合征(SCID)的小鼠在T细胞和B细胞成熟方面均表现出损伤,而骨髓生成则不受影响。我们在此报告,SCID小鼠的脾脏中带有NK细胞特征性的NK-2和去唾液酸GM1标记的细胞发生了表型扩增(70%-80%),并且这种扩增伴随着其正常C.B-17同窝小鼠的NK细胞溶解活性富集3至4倍。此外,SCID小鼠的NK细胞不会重排或表达T细胞受体α或β基因,也不会重排或表达第三个T细胞重排基因γ。这些发现表明:(a)T细胞受体对于NK介导的细胞溶解不是必需的;(b)NK细胞要么构成一个完全不同的谱系,要么NK细胞功能是在T细胞受体基因表达之前在T前体细胞中获得的。