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dc.contributor.authorBösl, Korbinian
dc.contributor.authorGiambelluca, Miriam
dc.contributor.authorHaug, Markus
dc.contributor.authorBugge, Marit
dc.contributor.authorEspevik, Terje
dc.contributor.authorKandasamy, Richard Kumaran
dc.contributor.authorBergstrøm, Bjarte Aune
dc.description.abstractInnate immune signaling is essential to mount a fast and specific immune response to pathogens. Monocytes and macrophages are essential cells in the early response in their capacity as ubiquitous phagocytic cells. They phagocytose microorganisms or damaged cells and sense pathogen/damage-associated molecular patterns (PAMPs/DAMPs) through innate receptors such as Toll-like receptors (TLRs). We investigated a phenomenon where co-signaling from TLR2 and TLR8 in human primary monocytes provides a distinct immune activation profile compared to signaling from either TLR alone. We compare gene signatures induced by either stimulus alone or together and show that co-signaling results in downstream differences in regulation of signaling and gene transcription. We demonstrate that these differences result in altered cytokine profiles between single and multi-receptor signaling, and show how it can influence both T-cell and neutrophil responses. The end response is tailored to combat extracellular pathogens, possibly by modifying the regulation of IFNβ and IL12-family cytokines.nb_NO
dc.publisherFrontiers Medianb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.titleCoactivation of TLR2 and TLR8 in Primary Human Monocytes Triggers a Distinct Inflammatory Signaling Responsenb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.source.journalFrontiers in Physiologynb_NO
dc.description.localcodeCopyright © 2018 Bösl, Giambelluca, Haug, Bugge, Espevik, Kandasamy and Bergstrøm. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).nb_NO
cristin.unitnameInstitutt for klinisk og molekylær medisin

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