Homozygous scid/scid;beige/beige mice have low levels of spontaneous or neonatal T cell-induced B cell generation.
Homozygous scid/scid;beige/beige mice have low levels of spontaneous or neonatal T cell-induced B cell generation.
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DOI：
10.1084/jem.177.1.191
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发表时间：
1993-01-01
影响因子：
15.3
通讯作者：
Gilmore, G L
中科院分区：
文献类型：
--
作者：
Mosier, D E;Stell, K L;Gulizia, R J;Torbett, B E;Gilmore, G L
常染色体隐性scid突变导致免疫球蛋白和T细胞受体基因重排缺陷。scid突变发生在同种异型同源的C.B-17细胞系中，高达25%的C.B-17 scid小鼠自发产生T细胞和免疫球蛋白，这种表型被称为“漏型”。此外，将新生T细胞引入C.B-17 scid小鼠可使100%的动物产生免疫球蛋白。我们已经产生了scid和beige突变的纯合小鼠。与c . b . 17小鼠相比，BALB/c。米色小鼠的“渗漏”发生率< 2%。这个百分比不会随着年龄的增长而增加，并且新生儿T细胞的引入不能挽救免疫球蛋白的产生。这表明与米色位点密切相关的一个或多个基因调控着B细胞和/或T细胞的发育。
The autosomal recessive scid mutation results in defective immunoglobulin and T cell receptor gene rearrangement. The scid mutation occurred in the allotype congenic C.B-17 line, and up to 25% of C.B-17 scid mice spontaneously produce both T cells and immunoglobulin, a phenotype known as "leaky." Moreover, introduction of neonatal T cells into C.B-17 scid mice leads to immunoglobulin production by 100% of animals. We have produced mice homozygous for both the scid and beige mutations. By contrast with C.B-17 scid mice, BALB/c scid.beige mice have a < 2% incidence of "leakiness." This percentage does not increase with age, and introduction of neonatal T cells fails to rescue immunoglobulin production. This suggests that a gene (or genes) closely linked to the beige locus regulates B and/or T cell development.