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-Aβ-chain gene of Ia-encoding region, the T-cell-receptor β (TcRβ)-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.
|Original language||English (US)|
|Number of pages||4|
|Journal||Proceedings of the National Academy of Sciences of the United States of America|
|State||Published - 1987|
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