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ZBP1 promotes LPS-induced cell death and IL-1β release via RHIM-mediated interactions with RIPK1
Inflammation and cell death are closely linked arms of the host immune response to infection, which when carefully balanced ensure host survival. One example of this balance is the tightly regulated transition from TNFR1-associated pro-inflammatory complex I to pro-death complex II. By contrast, her...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7782486/ https://www.ncbi.nlm.nih.gov/pubmed/33397971 http://dx.doi.org/10.1038/s41467-020-20357-z |
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author | Muendlein, Hayley I. Connolly, Wilson M. Magri, Zoie Smirnova, Irina Ilyukha, Vladimir Gautam, Avishekh Degterev, Alexei Poltorak, Alexander |
author_facet | Muendlein, Hayley I. Connolly, Wilson M. Magri, Zoie Smirnova, Irina Ilyukha, Vladimir Gautam, Avishekh Degterev, Alexei Poltorak, Alexander |
author_sort | Muendlein, Hayley I. |
collection | PubMed |
description | Inflammation and cell death are closely linked arms of the host immune response to infection, which when carefully balanced ensure host survival. One example of this balance is the tightly regulated transition from TNFR1-associated pro-inflammatory complex I to pro-death complex II. By contrast, here we show that a TRIF-dependent complex containing FADD, RIPK1 and caspase-8 (that we have termed the TRIFosome) mediates cell death in response to Yersinia pseudotuberculosis and LPS. Furthermore, we show that constitutive binding between ZBP1 and RIPK1 is essential for the initiation of TRIFosome interactions, caspase-8-mediated cell death and inflammasome activation, thus positioning ZBP1 as an effector of cell death in the context of bacterial blockade of pro-inflammatory signaling. Additionally, our findings offer an alternative to the TNFR1-dependent model of complex II assembly, by demonstrating pro-death complex formation reliant on TRIF signaling. |
format | Online Article Text |
id | pubmed-7782486 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-77824862021-01-11 ZBP1 promotes LPS-induced cell death and IL-1β release via RHIM-mediated interactions with RIPK1 Muendlein, Hayley I. Connolly, Wilson M. Magri, Zoie Smirnova, Irina Ilyukha, Vladimir Gautam, Avishekh Degterev, Alexei Poltorak, Alexander Nat Commun Article Inflammation and cell death are closely linked arms of the host immune response to infection, which when carefully balanced ensure host survival. One example of this balance is the tightly regulated transition from TNFR1-associated pro-inflammatory complex I to pro-death complex II. By contrast, here we show that a TRIF-dependent complex containing FADD, RIPK1 and caspase-8 (that we have termed the TRIFosome) mediates cell death in response to Yersinia pseudotuberculosis and LPS. Furthermore, we show that constitutive binding between ZBP1 and RIPK1 is essential for the initiation of TRIFosome interactions, caspase-8-mediated cell death and inflammasome activation, thus positioning ZBP1 as an effector of cell death in the context of bacterial blockade of pro-inflammatory signaling. Additionally, our findings offer an alternative to the TNFR1-dependent model of complex II assembly, by demonstrating pro-death complex formation reliant on TRIF signaling. Nature Publishing Group UK 2021-01-04 /pmc/articles/PMC7782486/ /pubmed/33397971 http://dx.doi.org/10.1038/s41467-020-20357-z Text en © 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/. |
spellingShingle | Article Muendlein, Hayley I. Connolly, Wilson M. Magri, Zoie Smirnova, Irina Ilyukha, Vladimir Gautam, Avishekh Degterev, Alexei Poltorak, Alexander ZBP1 promotes LPS-induced cell death and IL-1β release via RHIM-mediated interactions with RIPK1 |
title | ZBP1 promotes LPS-induced cell death and IL-1β release via RHIM-mediated interactions with RIPK1 |
title_full | ZBP1 promotes LPS-induced cell death and IL-1β release via RHIM-mediated interactions with RIPK1 |
title_fullStr | ZBP1 promotes LPS-induced cell death and IL-1β release via RHIM-mediated interactions with RIPK1 |
title_full_unstemmed | ZBP1 promotes LPS-induced cell death and IL-1β release via RHIM-mediated interactions with RIPK1 |
title_short | ZBP1 promotes LPS-induced cell death and IL-1β release via RHIM-mediated interactions with RIPK1 |
title_sort | zbp1 promotes lps-induced cell death and il-1β release via rhim-mediated interactions with ripk1 |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7782486/ https://www.ncbi.nlm.nih.gov/pubmed/33397971 http://dx.doi.org/10.1038/s41467-020-20357-z |
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