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. 2018 Apr 19;9:1560. doi: 10.1038/s41467-018-03669-z

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© The Author(s) 2018

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. 9 — Schematic representation of Pellino2 mediated NLRP3 inflammasome priming. In wild type macrophages LPS promotes the association of Pellino2 with NLRP3 and so facilitates ubiquitination of NLRP3. This promotes NLRP3 inflammasome assembly, ASC oligomerization and downstream caspase-1-mediated processing of pro-IL-1β and pro-IL-18 and pyroptosis. Pellino2 also promotes ubiquitination of IRAK1 and so limits the interaction of IRAK1 with NLRP3 and prevents the inhibitory effects of IRAK1 on NLRP3 activation. In Peli2^−/− macrophages this braking effect of Pellino2 on IRAK1 is removed, allowing for IRAK1 to interact with NLRP3 and suppress downstream activation of the NLRP3 inflammasome