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dc.contributor.authorAndrade, Warrison A
dc.contributor.authorAgarwal, Sarika
dc.contributor.authorMo, Shunyan
dc.contributor.authorShaffer, Scott A
dc.contributor.authorDillard, Joseph P
dc.contributor.authorSchmidt, Tobias
dc.contributor.authorHornung, Veit
dc.contributor.authorFitzgerald, Katherine A.
dc.contributor.authorKurt-Jones, Evelyn A.
dc.contributor.authorGolenbock, Douglas T
dc.date.accessioned2018-01-03T08:29:55Z
dc.date.available2018-01-03T08:29:55Z
dc.date.created2016-12-12T14:32:09Z
dc.date.issued2016
dc.identifier.citationCell reports. 2016, 15 (11), 2438-2448.nb_NO
dc.identifier.issn2211-1247
dc.identifier.urihttp://hdl.handle.net/11250/2474202
dc.description.abstractThe innate immune system is the first line of defense against Neisseria gonorrhoeae (GC). Exposure of cells to GC lipooligosaccharides induces a strong immune response, leading to type I interferon (IFN) production via TLR4/MD-2. In addition to living freely in the extracellular space, GC can invade the cytoplasm to evade detection and elimination. Double-stranded DNA introduced into the cytosol binds and activates the enzyme cyclic-GMP-AMP synthase (cGAS), which produces 2′3′-cGAMP and triggers STING/TBK-1/IRF3 activation, resulting in type I IFN expression. Here, we reveal a cytosolic response to GC DNA that also contributes to type I IFN induction. We demonstrate that complete IFN-β induction by live GC depends on both cGAS and TLR4. Type I IFN is detrimental to the host, and dysregulation of iron homeostasis genes may explain lower bacteria survival in cGAS−/− and TLR4−/− cells. Collectively, these observations reveal cooperation between TLRs and cGAS in immunity to GC infection.nb_NO
dc.language.isoengnb_NO
dc.publisherElseviernb_NO
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/deed.no*
dc.titleType I Interferon Induction by Neisseria gonorrhoeae: Dual Requirement of Cyclic GMP-AMP Synthase and Toll-like Receptor 4nb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.description.versionpublishedVersionnb_NO
dc.source.pagenumber2438-2448nb_NO
dc.source.volume15nb_NO
dc.source.journalCell reportsnb_NO
dc.source.issue11nb_NO
dc.identifier.doi10.1016/j.celrep.2016.05.030
dc.identifier.cristin1411595
dc.relation.projectNorges forskningsråd: 223255nb_NO
dc.description.localcode© 2016 The Authors. Published by Elsevier Ltd. This is an open access article under the CC-BY-NC-ND 4.0 license (http://creativecommons.org/licenses/by-nc-nd/4.0/)nb_NO
cristin.unitcode194,65,15,0
cristin.unitnameInstitutt for klinisk og molekylær medisin
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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Attribution-NonCommercial-NoDerivatives 4.0 Internasjonal
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