首页> 外文期刊>The Journal of Experomental Medicine >Homozygous scid/scid;beige/beige mice have low levels of spontaneous or neonatal T cell-induced B cell generation.
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Homozygous scid/scid;beige/beige mice have low levels of spontaneous or neonatal T cell-induced B cell generation.

机译:纯合scid / scid; beige / beige小鼠自发或新生T细胞诱导的B细胞生成水平较低。

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摘要

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.
机译:常染色体隐性scid突变导致免疫球蛋白缺陷和T细胞受体基因重排。 scid突变发生在同种异体的同基因C.B-17品系中,高达25%的C.B-17 scid小鼠自发产生T细胞和免疫球蛋白,即“泄漏”表型。此外,将新生的T细胞引入C.B-17 scid小鼠会导致100%的动物产生免疫球蛋白。我们已经为scid和米色突变产生了纯合小鼠。与C.B-17 scid小鼠相反,BALB / c scid.beige小鼠的“渗出”发生率小于2%。该百分比不会随年龄增加,并且引入新生儿T细胞无法挽救免疫球蛋白的产生。这表明与米色基因座紧密相连的一个或多个基因调节B和/或T细胞的发育。

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