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Isolevuglandins disrupt PU.1 mediated C1q expression and promote autoimmunity and hypertension in systemic lupus erythematosus

ABSTRACT: To determine the gene expression of profile of dendritic cells (DCs) from lupus prone mice we sorted CD11c+ cells from 4 7 week old female C57Bl/6 mice and 4 7 week old B6.SLE123 mice. We then performed gene expression profiling analysis using data obtained from RNA-seq from DCs of these 8 animals.

ORGANISM(S): Mus musculus

PROVIDER: GSE200485 | GEO | 2022/04/13

REPOSITORIES: GEO

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Isolevuglandins disrupt PU.1-mediated C1q expression and promote autoimmunity and hypertension in systemic lupus erythematosus.

Project description: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.

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Isolevuglandins disrupt PU.1 mediated C1q expression and promote autoimmunity and hypertension in systemic lupus erythematosus

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