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- W1669134410 abstract "Abstract Autoreactivity in lupus requires the delivery of autoantigens to APCs in a proinflammatory context. It has been proposed that apoptotic cells are a source of lupus autoantigens and targets for autoantibodies. Using a histone H2B-GFP fusion protein as traceable Ag, we show here that lupus autoantibodies, directed against nuclear autoantigens, can opsonize apoptotic cells, enhance their uptake through induction of proinflammatory FcγR-mediated phagocytosis, and augment Ag-specific T cell proliferation by increasing Ag loading. Apoptotic blebs and bodies seemed to be a preferred target of DC phagocytosis, via both “eat-me signals” and FcγR-mediated mechanisms; furthermore, inhibition of nuclear Ag redistribution, by blockade of chromatin fragmentation, could stop binding and opsonization of apoptotic cells by autoantibodies, and inhibited Fcγ-R-mediated enhancement of phagocytosis. Our results suggest that DC uptake of opsonized histones and other nuclear Ags from apoptotic cells is a novel pathway for the presentation of nuclear Ags in a highly inflammatory context. Blockade of chromatin fragmentation in lupus is a potential therapeutic approach, which could theoretically limit DC access to autoantigens delivered in proinflammatory context, while leaving available for tolerization those delivered in a noninflammatory context." @default.
- W1669134410 created "2016-06-24" @default.
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- W1669134410 date "2005-08-15" @default.
- W1669134410 modified "2023-10-16" @default.
- W1669134410 title "Nuclear Autoantigen Translocation and Autoantibody Opsonization Lead to Increased Dendritic Cell Phagocytosis and Presentation of Nuclear Antigens: A Novel Pathogenic Pathway for Autoimmunity?" @default.
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- W1669134410 doi "https://doi.org/10.4049/jimmunol.175.4.2692" @default.
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