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dc.contributor.authorBudden, Christina F.
dc.contributor.authorGearing, Linden J.
dc.contributor.authorKaiser, Romina
dc.contributor.authorStandke, Lena
dc.contributor.authorHertzog, Paul J.
dc.contributor.authorLatz, Eicke
dc.date2022-08-11T08:10:01.000
dc.date.accessioned2022-08-23T16:52:38Z
dc.date.available2022-08-23T16:52:38Z
dc.date.issued2021-08-02
dc.date.submitted2022-03-07
dc.identifier.citation<p>Budden CF, Gearing LJ, Kaiser R, Standke L, Hertzog PJ, Latz E. Inflammasome-induced extracellular vesicles harbour distinct RNA signatures and alter bystander macrophage responses. J Extracell Vesicles. 2021 Aug;10(10):e12127. doi: 10.1002/jev2.12127. Epub 2021 Aug 2. PMID: 34377374; PMCID: PMC8329986. <a href="https://doi.org/10.1002/jev2.12127">Link to article on publisher's site</a></p>
dc.identifier.issn2001-3078 (Linking)
dc.identifier.doi10.1002/jev2.12127
dc.identifier.pmid34377374
dc.identifier.urihttp://hdl.handle.net/20.500.14038/42093
dc.description.abstractInfectious organisms and damage of cells can activate inflammasomes, which mediate tissue inflammation and adaptive immunity. These mechanisms evolved to curb the spread of microbes and to induce repair of the damaged tissue. Chronic activation of inflammasomes, however, contributes to non-resolving inflammatory responses that lead to immuno-pathologies. Inflammasome-activated cells undergo an inflammatory cell death associated with the release of potent pro-inflammatory cytokines and poorly characterized extracellular vesicles (EVs). Since inflammasome-induced EVs could signal inflammasome pathway activation in patients with chronic inflammation and modulate bystander cell activation, we performed a systems analysis of the ribonucleic acid (RNA) content and function of two EV classes. We show that EVs released from inflammasome-activated macrophages carry a specific RNA signature and contain interferon beta (IFNbeta). EV-associated IFNbeta induces an interferon signature in bystander cells and results in dampening of NLRP3 inflammasome responses. EVs could, therefore, serve as biomarkers for inflammasome activation and act to prevent systemic hyper-inflammatory states by restricting NLRP3 activation in bystander cells.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=34377374&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright © 2021 The Authors. Journal of Extracellular Vesicles published by Wiley Periodicals, LLC on behalf of the International Society for Extracellular Vesicles. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectcell communication
dc.subjectextracellular vesicle
dc.subjectinflammasome
dc.subjectinflammation
dc.subjectinterferon β
dc.subjectnucleotide‐binding oligomerization domain (NOD)‐containing protein with a pyrin domain (NLRP3)
dc.subjectpyroptosis
dc.subjectCell Biology
dc.subjectImmunology and Infectious Disease
dc.titleInflammasome-induced extracellular vesicles harbour distinct RNA signatures and alter bystander macrophage responses
dc.typeJournal Article
dc.source.journaltitleJournal of extracellular vesicles
dc.source.volume10
dc.source.issue10
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=5929&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/4895
dc.identifier.contextkey28318796
refterms.dateFOA2022-08-23T16:52:38Z
html.description.abstract<p>Infectious organisms and damage of cells can activate inflammasomes, which mediate tissue inflammation and adaptive immunity. These mechanisms evolved to curb the spread of microbes and to induce repair of the damaged tissue. Chronic activation of inflammasomes, however, contributes to non-resolving inflammatory responses that lead to immuno-pathologies. Inflammasome-activated cells undergo an inflammatory cell death associated with the release of potent pro-inflammatory cytokines and poorly characterized extracellular vesicles (EVs). Since inflammasome-induced EVs could signal inflammasome pathway activation in patients with chronic inflammation and modulate bystander cell activation, we performed a systems analysis of the ribonucleic acid (RNA) content and function of two EV classes. We show that EVs released from inflammasome-activated macrophages carry a specific RNA signature and contain interferon beta (IFNbeta). EV-associated IFNbeta induces an interferon signature in bystander cells and results in dampening of NLRP3 inflammasome responses. EVs could, therefore, serve as biomarkers for inflammasome activation and act to prevent systemic hyper-inflammatory states by restricting NLRP3 activation in bystander cells.</p>
dc.identifier.submissionpathoapubs/4895
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology
dc.source.pagese12127


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Copyright © 2021 The Authors. Journal of Extracellular Vesicles published by Wiley Periodicals, LLC on behalf of the International Society for Extracellular Vesicles. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Except where otherwise noted, this item's license is described as Copyright © 2021 The Authors. Journal of Extracellular Vesicles published by Wiley Periodicals, LLC on behalf of the International Society for Extracellular Vesicles. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.