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γδ-T cells promote IFN-γ–dependent Plasmodium pathogenesis upon liver-stage infection

2019-04Journal article Restricted access
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dc.contributor.authorRibot, Julie C.
dc.contributor.authorNeres, Rita
dc.contributor.authorZuzarte-Luís, Vanessa
dc.contributor.authorGomes, Anita Quintal
dc.contributor.authorMancio-Silva, Liliana
dc.contributor.authorMensurado, Sofia
dc.contributor.authorPinto-Neves, Daniel
dc.contributor.authorSantos, Miguel M.
dc.contributor.authorCarvalho, Tânia
dc.contributor.authorLandry, Jonathan J. M.
dc.contributor.authorRolo, Eva A.
dc.contributor.authorMalik, Ankita
dc.contributor.authorSilva, Daniel Varón
dc.contributor.authorMota, Maria M.
dc.contributor.authorSilva-Santos, Bruno
dc.contributor.authorPamplona, Ana
dc.date.accessioned2019-05-14T14:00:45Z
dc.date.available2019-05-14T14:00:45Z
dc.date.issued2019-04
dc.description.abstractCerebral malaria (CM) is a major cause of death due to Plasmodium infection. Both parasite and host factors contribute to the onset of CM, but the precise cellular and molecular mechanisms that contribute to its pathogenesis remain poorly characterized. Unlike conventional αβ-T cells, previous studies on murine γδ-T cells failed to identify a nonredundant role for this T cell subset in experimental cerebral malaria (ECM). Here we show that mice lacking γδ-T cells are resistant to ECM when infected with Plasmodium berghei ANKA sporozoites, the liver-infective form of the parasite and the natural route of infection, in contrast with their susceptible phenotype if challenged with P. berghei ANKA-infected red blood cells that bypass the liver stage of infection. Strikingly, the presence of γδ-T cells enhanced the expression of Plasmodium immunogenic factors and exacerbated subsequent systemic and brain-infiltrating inflammatory αβ-T cell responses. These phenomena were dependent on the proinflammatory cytokine IFN-γ, which was required during liver stage for modulation of the parasite transcriptome, as well as for downstream immune-mediated pathology. Our work reveals an unanticipated critical role of γδ-T cells in the development of ECM upon Plasmodium liver-stage infection.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationRibot JC, Neres R, Zuzarte-Luís V, Gomes AQ, Mancio-Silva L, Mensurado S, et al. γδ-T cells promote IFN-γ-dependent Plasmodium pathogenesis upon liver-stage infection. Proc Natl Acad Sci U S A. 2019;116(20):9979-88.pt_PT
dc.identifier.doi10.1073/pnas.1814440116pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.21/10008
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherNational Academy of Sciencespt_PT
dc.relation.publisherversionhttps://www.pnas.org/content/early/2019/04/25/1814440116/tab-article-infopt_PT
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/pt_PT
dc.subjectPlasmodiumpt_PT
dc.subjectCerebral malariapt_PT
dc.subjectGamma-delta T cellspt_PT
dc.subjectInterferon-gammapt_PT
dc.subjectLiver stagept_PT
dc.titleγδ-T cells promote IFN-γ–dependent Plasmodium pathogenesis upon liver-stage infectionpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage9988pt_PT
oaire.citation.issue20pt_PT
oaire.citation.startPage201814440pt_PT
oaire.citation.startPage9978pt_PT
oaire.citation.titleProceedings of the National Academy of Sciencespt_PT
oaire.citation.volume116pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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