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- W3018484709 startingPage "6" @default.
- W3018484709 abstract "Currently, we have a limited understanding of mechanisms leading to systemic lupus erythematosus, but we know that genetics, environmental factors, and epigenetics contribute to the disease. One common aspect of the various environmental triggers is that they can cause cellular stress. When extraordinary stress occurs, such as viral activation, a cell's response can include increased nucleolar volume and activity to produce more machinery (e.g., ribosomes) to help the cell recover. However, nucleolar expansion can disrupt the epigenetic control in neighboring heterochromatin that comprises the nucleolar shell. This disruption can open underlying vulnerabilities that provoke an autoimmune reaction. Here, we review the X chromosome-nucleolus nexus hypothesis, which explains how nucleolar stress can disrupt epigenetically silenced chromatin, especially the neighboring inactive X chromosome (aka the nucleolar satellite). Chromatin disruption can lead to the expression of sequestered DNA, such as Alu elements and fully functional LINE-1 reverse transcriptase genes. In addition, Alu transcripts can disrupt the nucleolar structural integrity, leading to nucleolar disintegration. Such disintegration can leave nucleolar components and products in autoantigenic forms, such as abnormal conformations or incomplete macromolecular assemblies. Recent research on DNA sensing pathways can now be incorporated into the hypothesis to provide further details explaining how autoantibodies to endogenous nucleic acids arise." @default.
- W3018484709 created "2020-05-01" @default.
- W3018484709 creator A5040253164 @default.
- W3018484709 date "2020-04-23" @default.
- W3018484709 modified "2023-10-10" @default.
- W3018484709 title "An Epigenetics-Based Hypothesis of Autoantigen Development in Systemic Lupus Erythematosus" @default.
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