Mostrar el registro sencillo del ítem
dc.contributor.author | Pérez-Cabezas, Begoña | |
dc.contributor.author | Cecílio, Pedro | |
dc.contributor.author | Robalo, Ana Luisa | |
dc.contributor.author | Silvestre, Ricardo | |
dc.contributor.author | Carrillo, Eugenia | |
dc.contributor.author | Moreno, Javier | |
dc.contributor.author | San Martín, Juan Víctor | |
dc.contributor.author | Vasconcellos, Rita | |
dc.contributor.author | Cordeiro-da-Silva, Anabela | |
dc.date.accessioned | 2020-01-29T11:44:05Z | |
dc.date.available | 2020-01-29T11:44:05Z | |
dc.date.issued | 2016 | |
dc.identifier.citation | Front Immunol. 2016 Nov 4;7:478. eCollection 2016. | es_ES |
dc.identifier.issn | 1664-3224 | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/8960 | |
dc.description.abstract | The complexity of Leishmania-host interactions, one of the main leishmaniasis issues, is yet to be fully understood. We detected elevated IL-27 plasma levels in European patients with active visceral disease caused by Leishmania infantum, which returned to basal levels after successful treatment, suggesting this cytokine as a probable infection mediator. We further addressed this hypothesis recurring to two classical susceptible visceral leishmaniasis mouse models. BALB/c, but not C57BL/6 mice, showed increased IL-27 systemic levels after infection, which was associated with an upregulation of IL-27p28 expression by dendritic cells and higher parasite burdens. Neutralization of IL-27 in acutely infected BALB/c led to decreased parasite burdens and a transient increase in IFN-γ+ splenic T cells, while administration of IL-27 to C57BL/6 promoted a local anti-inflammatory cytokine response at the site of infection and increased parasite loads. Overall, we show that, as in humans, BALB/c IL-27 systemic levels are infection dependently upregulated and may favor parasite installation by controlling inflammation. | es_ES |
dc.description.sponsorship | This work was supported by Fundação para a Ciência e Tecnologia (FCT)/Ministério da Educação e da Ciência (MEC), co-funded by FEDER under the PT2020 Partnership Agreement through the Research Unit NO. 4293; by European Community’s Seventh Framework Programme under grant agreement No. 603182 (Project MuLeVaClin) and by the ISCIII-AES project (project reference PI13/00440). PC and BP-C are supported by fellowships from the European Community’s Seventh Framework Programme under grant agreements No. 603182 (Project MuLeVaClin) and No. 603240-2 (Project NMTryPI), respectively. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Frontiers Media | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject | IL-27 | es_ES |
dc.subject | Leishmania infantum | es_ES |
dc.subject | Human | es_ES |
dc.subject | Immune regulation | es_ES |
dc.subject | Mouse models | es_ES |
dc.title | Interleukin-27 Early Impacts Leishmania infantum Infection in Mice and Correlates with Active Visceral Disease in Humans | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Atribución 4.0 Internacional | * |
dc.identifier.pubmedID | 27867384 | es_ES |
dc.format.volume | 7 | es_ES |
dc.format.page | 478 | es_ES |
dc.identifier.doi | 10.3389/fimmu.2016.00478 | es_ES |
dc.contributor.funder | Fundação para a Ciência e Tecnologia (Portugal) | |
dc.contributor.funder | Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) | |
dc.contributor.funder | Unión Europea. Comisión Europea | |
dc.description.peerreviewed | Sí | es_ES |
dc.relation.publisherversion | https://doi.org/10.3389/fimmu.2016.00478 | es_ES |
dc.identifier.journal | Frontiers in immunology | es_ES |
dc.repisalud.centro | ISCIII::Centro Nacional de Microbiología | es_ES |
dc.repisalud.institucion | ISCIII | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/PI13/00440 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/Seventh Framework No. 603182 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/ PI13/00440 | es_ES |
dc.rights.accessRights | open access | es_ES |