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. 2022 Jan 7;19(4):453–455. doi: 10.1038/s41423-021-00817-2

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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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Impact of epithelial NELF on transcriptional regulation of cell junction proteins in murine IEC. Epithelial NELF ensure sufficient expression of the cell junction proteins Cldn3, Cldn23 and Cgn. IEC-specific NELF-deficiency compromises the expression of Cldn3, Cldn23, and Cgn and promotes IEC necroptosis without obvious effects on intestinal barrier integrity. DSS-induced intestinal inflammation combined with IEC-specific NELF-deficiency, however, exacerbates intestinal inflammation by enhancing impairment of cell junction protein expression, IEC necroptosis, and consequently bacterial translocation from the intestinal lumen into the deeper gut tissue. Protein structures are symbolic. (Created with BioRender.com)