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• W2016899230 abstract "Indirect evidence suggests that type-I interferons (IFN-alpha/beta) play a significant role in the pathogenesis of lupus. To directly examine the contribution of these pleiotropic molecules, we created congenic NZB mice lacking the alpha-chain of IFN-alpha/betaR, the common receptor for the multiple IFN-alpha/beta species. Compared with littermate controls, homozygous IFN-alpha/betaR-deleted NZB mice had significantly reduced anti-erythrocyte autoantibodies, erythroblastosis, hemolytic anemia, anti-DNA autoantibodies, kidney disease, and mortality. These reductions were intermediate in the heterozygous-deleted mice. The disease-ameliorating effects were accompanied by reductions in splenomegaly and in several immune cell subsets, including B-1 cells, the major producers of anti-erythrocyte autoantibodies. Decreases of B and T cell proliferation in vitro and in vivo, and of dendritic cell maturation and T cell stimulatory activity in vitro were also detected. Absence of signaling through the IFN-alpha/betaR, however, did not affect increased basal levels of the IFN-responsive p202 phosphoprotein, encoded by a polymorphic variant of the Ifi202 gene associated with the Nba2 predisposing locus in NZB mice. The data indicate that type-I IFNs are important mediators in the pathogenesis of murine lupus, and that reducing their activity in the human counterpart may be beneficial." @default.
• W2016899230 created "2016-06-24" @default.
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• W2016899230 date "2003-03-17" @default.
• W2016899230 modified "2023-10-17" @default.
• W2016899230 title "Type-I Interferon Receptor Deficiency Reduces Lupus-like Disease in NZB Mice" @default.
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• W2016899230 doi "https://doi.org/10.1084/jem.20021996" @default.
• W2016899230 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2193854" @default.
• W2016899230 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12642605" @default.
• W2016899230 hasPublicationYear "2003" @default.
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