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dc.contributor.authorMeås, Hany Zakaria
dc.contributor.authorHaug, Markus
dc.contributor.authorBeckwith, Marianne Sandvold
dc.contributor.authorLouet, Claire
dc.contributor.authorRyan, Liv
dc.contributor.authorHu, Zhenyi
dc.contributor.authorLandskron, Johannes
dc.contributor.authorNordbø, Svein Arne
dc.contributor.authorTasken, Kjetil
dc.contributor.authorYin, Hang
dc.contributor.authorDamås, Jan Kristian
dc.contributor.authorFlo, Trude Helen
dc.date.accessioned2020-01-27T08:09:57Z
dc.date.available2020-01-27T08:09:57Z
dc.date.created2020-01-17T09:12:24Z
dc.date.issued2020
dc.identifier.issn2041-1723
dc.identifier.urihttp://hdl.handle.net/11250/2637938
dc.description.abstractDuring HIV infection, cell-to-cell transmission results in endosomal uptake of the virus by target CD4+ T cells and potential exposure of the viral ssRNA genome to endosomal Toll-like receptors (TLRs). TLRs are instrumental in activating inflammatory responses in innate immune cells, but their function in adaptive immune cells is less well understood. Here we show that synthetic ligands of TLR8 boosted T cell receptor signaling, resulting in increased cytokine production and upregulation of surface activation markers. Adjuvant TLR8 stimulation, but not TLR7 or TLR9, further promoted T helper cell differentiation towards Th1 and Th17. In addition, we found that endosomal HIV induced cytokine secretion from CD4+ T cells in a TLR8-specific manner. TLR8 engagement also enhanced HIV-1 replication and potentiated the reversal of latency in patient-derived T cells. The adjuvant TLR8 activity in T cells can contribute to viral dissemination in the lymph node and low-grade inflammation in HIV patients. In addition, it can potentially be exploited for therapeutic targeting and vaccine development.nb_NO
dc.language.isoengnb_NO
dc.publisherNature Researchnb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleSensing of HIV-1 by TLR8 activates human T cells and reverses latencynb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.description.versionpublishedVersionnb_NO
dc.source.volume11nb_NO
dc.source.journalNature Communicationsnb_NO
dc.identifier.doihttps://doi.org/10.1038/s41467-019-13837-4
dc.identifier.cristin1775410
dc.relation.projectNorges forskningsråd: 223255nb_NO
dc.relation.projectSamarbeidsorganet mellom Helse Midt-Norge og NTNU: 90176000nb_NO
dc.description.localcode© 2020 The Authors. Published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License.nb_NO
cristin.unitcode194,65,15,0
cristin.unitnameInstitutt for klinisk og molekylær medisin
cristin.ispublishedtrue
cristin.fulltextpostprint
cristin.fulltextoriginal
cristin.qualitycode2


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Navngivelse 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse 4.0 Internasjonal