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- W4282934792 abstract "We describe a mechanism responsible for systemic lupus erythematosus (SLE). In humans with SLE and in 2 SLE murine models, there was marked enrichment of isolevuglandin-adducted proteins (isoLG adducts) in monocytes and dendritic cells. We found that antibodies formed against isoLG adducts in both SLE-prone mice and humans with SLE. In addition, isoLG ligation of the transcription factor PU.1 at a critical DNA binding site markedly reduced transcription of all C1q subunits. Treatment of SLE-prone mice with the specific isoLG scavenger 2-hydroxybenzylamine (2-HOBA) ameliorated parameters of autoimmunity, including plasma cell expansion, circulating IgG levels, and anti-dsDNA antibody titers. 2-HOBA also lowered blood pressure, attenuated renal injury, and reduced inflammatory gene expression uniquely in C1q-expressing dendritic cells. Thus, isoLG adducts play an essential role in the genesis and maintenance of systemic autoimmunity and hypertension in SLE." @default.
- W4282934792 created "2022-06-16" @default.
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- W4282934792 date "2022-07-08" @default.
- W4282934792 modified "2023-10-17" @default.
- W4282934792 title "Isolevuglandins disrupt PU.1-mediated C1q expression and promote autoimmunity and hypertension in systemic lupus erythematosus" @default.
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- W4282934792 doi "https://doi.org/10.1172/jci.insight.136678" @default.
- W4282934792 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35608913" @default.
- W4282934792 hasPublicationYear "2022" @default.
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