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. 2021 May 11;64(8):1805–1815. doi: 10.1007/s00125-021-05469-5

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© The Author(s) 2021

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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Fig. 5 — The activation and the feedback loop of the innate antiviral immune system during a viral infection. The RNA dysregulated genes/proteins where SNPs were also found in the GWAS study are highlighted in red. Genes/proteins that were only dysregulated at the RNA level are highlighted in green. SP1 is highlighted in yellow because we only found SNPs in this gene associated with type 1 diabetes. The figure illustrates the multitude of genes involved in the potential overactivation in response to an infection in type 1 diabetes. LPS, lipopolysaccharide