Flt3L-Mediated expansion of plasmacytoid dendritic cells suppresses HIV infection in humanized mice
dc.contributor.author | Pham, Tram N.Q. | |
dc.contributor.author | Meziane, Oussama | |
dc.contributor.author | Miah, Mohammad Alam | |
dc.contributor.author | Volodina, Olga | |
dc.contributor.author | Colas, Chloé | |
dc.contributor.author | Béland, Kathie | |
dc.contributor.author | Li, Yuanyi | |
dc.contributor.author | Dallaire, Frédéric | |
dc.contributor.author | Keler, Tibor | |
dc.contributor.author | Guimond, Jean V. | |
dc.contributor.author | Lesage, Sylvie | |
dc.contributor.author | Cheong, Cheolho | |
dc.contributor.author | Haddad, Elie | |
dc.contributor.author | Cohen, Éric A. | |
dc.date.accessioned | 2023-01-24T14:21:23Z | |
dc.date.available | NO_RESTRICTION | fr |
dc.date.available | 2023-01-24T14:21:23Z | |
dc.date.issued | 2019-11-26 | |
dc.identifier.uri | http://hdl.handle.net/1866/27342 | |
dc.publisher | Cell Press | fr |
dc.rights | Ce document est mis à disposition selon les termes de la Licence Creative Commons Attribution - Pas d’utilisation commerciale - Pas de Modification 4.0 International. / This work is licensed under a Creative Commons Attribution - NonCommercial - NoDerivatives 4.0 International License. | |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.fr | |
dc.subject | FLT3L | fr |
dc.subject | PDCs | fr |
dc.subject | Acute HIV infection | fr |
dc.subject | TLR7 stimulation | fr |
dc.subject | IFN-I | fr |
dc.subject | Antiviral response | fr |
dc.subject | PDC dysfunction | fr |
dc.subject | Hu-mice | fr |
dc.title | Flt3L-Mediated expansion of plasmacytoid dendritic cells suppresses HIV infection in humanized mice | fr |
dc.type | Article | fr |
dc.contributor.affiliation | Université de Montréal. Faculté de médecine. Département de microbiologie, infectiologie et immunologie | fr |
dc.identifier.doi | 10.1016/j.celrep.2019.10.094 | |
dcterms.abstract | Plasmacytoid dendritic cells (plasmacytoid DC, pDC) are major IFN-I producers and have been shown to be affected by HIV through ill-defined mechanisms. In this study, we directly assess the role of pDC in early infection, evaluating whether modulating their abundance can alter viral replication. First, HIV infection of humanized mice induces systemic depletion of pDC, and in the presence of soluble FMS-like tyrosine kinase 3 ligand (Flt3L), pDC levels remain elevated. Flt3L significantly delays the onset of viremia and reduces viral replication via a process that is dependent on pDC and mediated through an enhanced early IFN-I response. pDC from Flt3L-treated mice are more prone to express IFN-a following TLR7 stimulation, but this propensity is gradually decreased during infection. In conclusion, maintaining pDC levels and function is key to effective early viral control, and in this context, these findings provide practical insights for anti-HIV strategies and vaccine design. | fr |
dcterms.isPartOf | urn:ISSN:2211-1247 | fr |
dcterms.language | eng | fr |
UdeM.ReferenceFournieParDeposant | doi.org/10.1016/j.celrep.2019.10.094 | fr |
UdeM.VersionRioxx | Version publiée / Version of Record | fr |
oaire.citationTitle | Cell reports | fr |
oaire.citationVolume | 29 | fr |
oaire.citationIssue | 9 | fr |
oaire.citationStartPage | 2770 | fr |
oaire.citationEndPage | 2782 | fr |
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Droits d'utilisation : Ce document est mis à disposition selon les termes de la Licence Creative Commons Attribution - Pas d’utilisation commerciale - Pas de Modification 4.0 International. / This work is licensed under a Creative Commons Attribution - NonCommercial - NoDerivatives 4.0 International License.