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. 2020 Oct 6;10:16648. doi: 10.1038/s41598-020-73654-4

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Patterns of gene co-expression in SLE. Graphical representation of the most prominent characteristics of gene co-expression patterns. Healthy genomes have extended domains of co-ordinated gene expression (DCE), but these become shorter and more fragmented in the genomes of patients with low disease activity. A significant number of differentially expressed genes (DEGs) in SLE low-activity genomes are associated with a disease “susceptibility” signature, located in split DCEs, linked to interferon and other signaling pathways and enriched in regions of low chromatin accessibility. In high disease activity genomes DCEs are re-distributed in new regions, where genes linked a SLE “severity” signature and more generalized manifestations of the disease (e.g. nephritis) localize in areas of DCE contraction, depletion and overall increased chromatin accessibility.