首页> 外文OA文献 >T-cell-receptor beta- and I-A beta-chain genes of normal SWR mice are linked with the development of lupus nephritis in NZB x SWR crosses.
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T-cell-receptor beta- and I-A beta-chain genes of normal SWR mice are linked with the development of lupus nephritis in NZB x SWR crosses.

机译:正常SWR小鼠的T细胞受体β和I-Aβ链基因与NZB x SWR杂交中狼疮性肾炎的发展有关。

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摘要

The incidence of nephritis in autoimmune New Zealand Black (NZB) mice is low, but when they are crossed with normal SWR mice, almost 100% of the female F1 hybrids (SNF1) develop lethal glomerulonephritis. To define the contribution of the normal SWR strain to the development of nephritis, we analyzed the association of the I-A beta-chain gene of Ia-encoding region, the T-cell-receptor beta (TcR beta)-chain gene, and immunoglobulin heavy-chain allotype (IgH) with the development of lupus nephritis in 165 NZB X SWR crosses. We found that genes linked to the TcR and Ir gene loci of the normal SWR mice interacted with NZB-derived genes, leading to the development of accelerated and severe nephritis in the NZB X SWR crosses.
机译:自身免疫性新西兰黑(NZB)小鼠中肾炎的发生率较低,但是当它们与正常SWR小鼠杂交时,几乎100%的雌性F1杂种(SNF1)会发生致命性肾小球肾炎。为了定义正常SWR株对肾炎发展的贡献,我们分析了Ia编码区的IAβ链基因,T细胞受体β(TcR beta)链基因和免疫球蛋白重链的关联165 NZB X SWR杂交中狼疮性肾炎发生的双链异型(IgH)。我们发现与正常SWR小鼠的TcR和Ir基因位点相关的基因与NZB衍生的基因相互作用,导致NZB X SWR杂交中加速和严重肾炎的发展。

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