Engagement of Fas on macrophages modulates poly I:C induced cytokine production with specific enhancement of IP-10

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dc.contributor.author Lyons, Caitríona M. en
dc.contributor.author Fernandes, Philana en
dc.contributor.author Fanning, Liam J. en
dc.contributor.author Houston, Aileen M. en
dc.contributor.author Brint, Elizabeth K. en
dc.date.accessioned 2016-02-17T10:07:58Z
dc.date.available 2016-02-17T10:07:58Z
dc.date.issued 2015
dc.identifier.citation Lyons C, Fernandes P, Fanning LJ, Houston A, Brint E (2015) Engagement of Fas on Macrophages Modulates Poly I:C Induced Cytokine Production with Specific Enhancement of IP-10. PLoS ONE 10(4): e0123635. doi:10.1371/journal.pone.0123635
dc.identifier.volume 10 en
dc.identifier.issued 4 en
dc.identifier.issn 1932-6203
dc.identifier.uri http://hdl.handle.net/10468/2313
dc.identifier.doi 10.1371/journal.pone.0123635
dc.description.abstract Viral double-stranded RNA (dsRNA) is recognised by pathogen recognition receptors such as Toll-Like Receptor 3 (TLR3) and retinoic acid inducible gene-I (RIG-I), and results in cytokine and interferon production. Fas, a well characterised death receptor, has recently been shown to play a role in the inflammatory response. In this study we investigated the role of Fas in the anti-viral immune response. Stimulation of Fas on macrophages did not induce significant cytokine production. However, activation of Fas modified the response of macrophages to the viral dsRNA analogue poly I:C. In particular, poly I:C-induced IP-10 production was significantly enhanced. A similar augmentation of IP-10 by Fas was observed following stimulation with both poly A:U and Sendai virus. Fas activation suppressed poly I:C-induced phosphorylation of the MAP kinases p38 and JNK, while overexpression of the Fas adaptor protein, Fas-associated protein with death domain (FADD), activated AP-1 and inhibited poly I:C-induced IP-10 production. Consistent with an inhibitory role for AP-1 in IP-10 production, mutation of the AP-1 binding site on the IP-10 promoter resulted in augmented poly I:C-induced IP-10. These results demonstrate that engagement of the Fas receptor plays a role in modifying the innate immune response to viral RNA. en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Public Library of Science en
dc.rights © 2015 Lyons et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited en
dc.rights.uri http://creativecommons.org/licenses/by/4.0/ en
dc.subject NF-kappaB en
dc.subject Domain-containing protein en
dc.subject Hepatitis C virus en
dc.subject RIG-I en
dc.subject Death domain en
dc.subject Induced apoptosis en
dc.subject Infected cells en
dc.subject Activation en
dc.subject Fadd en
dc.subject IL-1 beta en
dc.title Engagement of Fas on macrophages modulates poly I:C induced cytokine production with specific enhancement of IP-10 en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother Aileen Houston, Department of Medicine, University College Cork, Cork, Ireland. +353-21-490-3000 Email: a.houston@ucc.ie en
dc.internal.availability Full text available en
dc.description.version Published Version en
dc.internal.rssid 348785913
dc.internal.wokid WOS:000352477800247
dc.contributor.funder Science Foundation Ireland en
dc.description.status Peer reviewed en
dc.identifier.journaltitle PLOS ONE en
dc.internal.IRISemailaddress a.houston@ucc.ie en
dc.identifier.articleid e0123635
dc.relation.project info:eu-repo/grantAgreement/SFI/SFI Research Frontiers Programme (RFP)/10/RFP/CAN2894/IE/Fas (CD95) signaling and cancer-associated inflammation/
dc.relation.project info:eu-repo/grantAgreement/SFI/SFI Research Frontiers Programme (RFP)/10/RFP/BIC2737/IE/Molecular mechanisms regulating Toll-Like Receptor signalling in Intestinal Epithelial Cells/


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© 2015 Lyons et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Except where otherwise noted, this item's license is described as © 2015 Lyons et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
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