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

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dc.contributor.authorRibot, Julie
dc.contributor.authorNeres, Rita
dc.contributor.authorZuzarte-Luis, Vanessa
dc.contributor.authorGomes, Anita Q.
dc.contributor.authorMancio-Silva, Liliana
dc.contributor.authorMensurado, Sofia
dc.contributor.authorNeves, Daniel
dc.contributor.authorMonteiro Dos Santos, Miguel
dc.contributor.authorCarvalho, Tânia
dc.contributor.authorLandry, Jonathan J. M.
dc.contributor.authorA. Rolo, Eva
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.accessioned2022-05-10T15:39:24Z
dc.date.available2022-05-10T15:39:24Z
dc.date.issued2019
dc.description© 2019. Published under the PNAS license.pt_PT
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.sponsorshipThis work was supported by Fundação para a Ciência e a Tecnologia (FCT) (PTDC/SAU-OSM/099ALTF 357-2009 and BPD-81953-2011, ALTF 960-2009, and PD/BD/114099/2015724/2008 to A.P.) and European Research Council (CoG_646701 to B.S.-S.). We also acknowledge UID/ BIM/50005/2019, a project funded by Fundação para a Ciência e a Tecnologia (FCT)/Ministério da Ciência, Tecnologia e Ensino Superior (MCTES) through Fundos do Orçamento de Estado. A.P. was supported by a Ciência 2008 position of the Portuguese Ministry of Science and Technology, supported by a FCT fellowship (SFRH/BPD/110380/2015), and currently holds a research position supported by FCT (under decree-law no. 57/2016 of July 19th, as amended by law no. 57/2017). J.C.R., R.N., V.Z.-L., L.M.-S., and S.M. were supported by individual fellowships from FCT and European Molecular Biology Organization Long-Term Fellowships (IF/00013/2014, SFRH/BI/51054/2010, SFRH/BPD/81953/2011, , respectively). L.M.-S. was also supported by the European Community’s Sev- enth Framework Programme (FP7/2007-2013) under Grant Agreement 242095 (EVIMalaR). Currently V.Z.-L. holds a research position supported by FCT (under decree-law no. 57/2016 of July 19th, as amended by law no. 57/2017), and J.C.R. holds a FCT investigator position (IF/00013/2014).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationProc Natl Acad Sci USA. 2019 May 14;116(20):9979-9988pt_PT
dc.identifier.doi10.1073/pnas.1814440116pt_PT
dc.identifier.eissn1091-6490
dc.identifier.issn0027-8424
dc.identifier.urihttp://hdl.handle.net/10451/52867
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherNational Academy of Sciencept_PT
dc.relationRelevance of Cholesterol - rich diet on protection from experimental cerebral malaria
dc.relationMicroRNA determinants of the balance between effector and regulatory T cells in vivo
dc.relationInstituto de Medicina Molecular
dc.relationThe role of liver stage-dependent innate lymphocytes in the pathogenesis of experimental cerebral malaria
dc.relationDeciphering the outside-in mechanisms of human gd T cell differentiation
dc.relationINTERMALTRAINING - INTERVENTION STRATEGIES AGAINST MALARIA
dc.relationMECHANISMS OF PLASMODIUM LIVER INFECTION: SUBVERTING THE HOST UBIQUITIN-PROTEASOME PATHWAY TOWARDS AN IMMUNE EVASION STRATEGY
dc.relationA designar
dc.relationTowards the establishment of a permanent European Virtual Institute dedicated to Malaria Research (EVIMalaR).
dc.relation.publisherversionhttps://www.pnas.org/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.awardTitleRelevance of Cholesterol - rich diet on protection from experimental cerebral malaria
oaire.awardTitleMicroRNA determinants of the balance between effector and regulatory T cells in vivo
oaire.awardTitleInstituto de Medicina Molecular
oaire.awardTitleThe role of liver stage-dependent innate lymphocytes in the pathogenesis of experimental cerebral malaria
oaire.awardTitleDeciphering the outside-in mechanisms of human gd T cell differentiation
oaire.awardTitleINTERMALTRAINING - INTERVENTION STRATEGIES AGAINST MALARIA
oaire.awardTitleMECHANISMS OF PLASMODIUM LIVER INFECTION: SUBVERTING THE HOST UBIQUITIN-PROTEASOME PATHWAY TOWARDS AN IMMUNE EVASION STRATEGY
oaire.awardTitleA designar
oaire.awardTitleTowards the establishment of a permanent European Virtual Institute dedicated to Malaria Research (EVIMalaR).
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PTDC%2FSAU-OSM%2F099724%2F2008/PT
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oaire.citation.endPage9988pt_PT
oaire.citation.issue20pt_PT
oaire.citation.startPage9979pt_PT
oaire.citation.titleProceedings of the National Academy of Sciencespt_PT
oaire.citation.volume116pt_PT
oaire.fundingStream3599-PPCDT
oaire.fundingStreamH2020
oaire.fundingStream6817 - DCRRNI ID
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rcaap.typearticlept_PT
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