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Systemic Lupus Erythematosus - U.S. Department of Veterans Affairs

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Last Updated: 27 July 2022

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

There was a significant increase of isolevuglandin-adducted proteins in monocytes and dendritic cells in humans with SLE and 2 SLE murine models. In both SLE-prone mice and humans with SLE, antibodies against isoLG adducts were found 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. In C1q-expressing dendritic cells, 2-HOBA reduced blood pressure, attenuated renal injury, and reduced inflammatory gene expression in C1q-expressing dendritic cells.

Source link: https://doi.org/10.1172/jci.insight.136678


A High Prevalence of Anti-EBNA1 Heteroantibodies in Systemic Lupus Erythematosus (SLE) Supports Anti-EBNA1 as an Origin for SLE Autoantibodies.

EBV has a mechanistic role in SLE pathogenesis, which is the challenge. EBV has been deciphered as a mediator of SLE pathogenesis, but it is impossible to state mechanistic roles. Four instances of autoantibody cross-reactions between SLE autoantigens and Epstein-Barr nuclear antigen 1 are found in our database. If this assumption is correct, anti-EB1 responses in EBV-infected SLE patients would be more frequent than in EBV-infected SLE patients than in EBV-infected controls.

Source link: https://doi.org/10.3389/fimmu.2022.830993

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions