Journal
JOURNAL OF IMMUNOLOGY
Volume 165, Issue 8, Pages 4190-4201Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.165.8.4190
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- NIAMS NIH HHS [AR/AI42732] Funding Source: Medline
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Of the multiple murine models of autoimmunity, the three most closely resembling human systemic lupus erythematosus (SLE) are the MRL/lpr, New Zealand Black/White F-1, and male BXSB, Although these strains share;many disease characteristics, no common cellular defect has previously been found in prediseased mice from all these strains. We show in this study that macrophages from prediseased mice of all three SLE-prone strains, as web as macrophages from mice whose genomes contribute to the development of SLE (MRL/+, New Zealand White, New Zealand Black, female BXSB, and LG/J), have an identical and profound defect in cytokine expression that is triggered by apoptotic cells, Strikingly, none of 13 nonautoimmune strains tested exhibited this defect. Given that apoptotic Ags have been increasingly recognized as the target of autoantibodies, a defect in cytokine expression that is triggered by apoptotic cells has broad potential to upset the balance between tolerance and immunity.
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