Neilson E G, Gasser D L, McCafferty E, Zakheim B, Phillips S M
Immunogenetics. 1983;17(1):55-65. doi: 10.1007/BF00364289.
Inbred strains of rats differ widely in their susceptibility to interstitial nephritis induced by rabbit renal tubular basement membrane (TBM) preparations. We now report that susceptibility is determined in part by an RT1-linked gene for effector cell responsiveness producing interstitial lesions. Furthermore, we also obtained evidence that the gene determining expression of the target TBM antigen is linked to the gene for albinism on the first linkage group. When non-susceptible rats lacking the TBM antigen but having the gene for cellular responsiveness were mated with non-susceptible rats which had the TBM antigen but lacked the gene for cellular responsiveness, the F1 hybrids were susceptible to the induction of interstitial nephritis. Although strains varied widely in the amount of anti-TBM antibody (alpha TBM-Ab) they produced, this variation does not appear to be controlled by RT1-linked genes, nor does the isotype or amount of antibody appear to be related to the susceptibility to infiltrating cellular lesions.
大鼠近交系对兔肾小管基底膜（TBM）制剂诱导的间质性肾炎的易感性差异很大。我们现在报告，易感性部分由一个与RT1连锁的基因决定，该基因负责产生间质性病变的效应细胞反应性。此外，我们还获得了证据，表明决定靶TBM抗原表达的基因与第一连锁群上的白化病基因相连。当缺乏TBM抗原但具有细胞反应性基因的非易感大鼠与具有TBM抗原但缺乏细胞反应性基因的非易感大鼠交配时，F1代杂种对间质性肾炎的诱导易感。尽管不同品系产生的抗TBM抗体（αTBM-Ab）量差异很大，但这种差异似乎不受与RT1连锁的基因控制，抗体的亚型或量似乎也与浸润性细胞病变的易感性无关。
