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

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dc.contributor.authorLyons, Caitríona M.en
dc.contributor.authorFernandes, Philanaen
dc.contributor.authorFanning, Liam J.en
dc.contributor.authorHouston, Aileen M.en
dc.contributor.authorBrint, Elizabeth K.en
dc.contributor.funderScience Foundation Irelanden
dc.date.accessioned2016-02-17T10:07:58Z
dc.date.available2016-02-17T10:07:58Z
dc.date.issued2015
dc.description.abstractViral 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.description.statusPeer revieweden
dc.description.versionPublished Versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.articleide0123635
dc.identifier.citationLyons 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.doi10.1371/journal.pone.0123635
dc.identifier.issn1932-6203
dc.identifier.issued4en
dc.identifier.journaltitlePLOS ONEen
dc.identifier.urihttps://hdl.handle.net/10468/2313
dc.identifier.volume10en
dc.language.isoenen
dc.publisherPublic Library of Scienceen
dc.relation.projectinfo:eu-repo/grantAgreement/SFI/SFI Research Frontiers Programme (RFP)/10/RFP/CAN2894/IE/Fas (CD95) signaling and cancer-associated inflammation/
dc.relation.projectinfo:eu-repo/grantAgreement/SFI/SFI Research Frontiers Programme (RFP)/10/RFP/BIC2737/IE/Molecular mechanisms regulating Toll-Like Receptor signalling in Intestinal Epithelial Cells/
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 crediteden
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectNF-kappaBen
dc.subjectDomain-containing proteinen
dc.subjectHepatitis C virusen
dc.subjectRIG-Ien
dc.subjectDeath domainen
dc.subjectInduced apoptosisen
dc.subjectInfected cellsen
dc.subjectActivationen
dc.subjectFadden
dc.subjectIL-1 betaen
dc.titleEngagement of Fas on macrophages modulates poly I:C induced cytokine production with specific enhancement of IP-10en
dc.typeArticle (peer-reviewed)en
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