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https://hdl.handle.net/1822/24093
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Campo DC | Valor | Idioma |
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dc.contributor.author | Carvalho, Agostinho | - |
dc.contributor.author | Giovannini, Gloria | - |
dc.contributor.author | De Luca, Antonella | - |
dc.contributor.author | D’Angelo, Carmen | - |
dc.contributor.author | Casagrande, Andrea | - |
dc.contributor.author | Iannitti, Rossana G. | - |
dc.contributor.author | Ricci, Giovanni | - |
dc.contributor.author | Cunha, Cristina | - |
dc.contributor.author | Romani, Luigina | - |
dc.date.accessioned | 2013-05-17T13:49:49Z | - |
dc.date.available | 2013-05-17T13:49:49Z | - |
dc.date.issued | 2012-05 | - |
dc.identifier.issn | 1672-7681 | por |
dc.identifier.uri | https://hdl.handle.net/1822/24093 | - |
dc.description | We thank Dr. Cristina Massi Benedetti for digital art and editing | por |
dc.description.abstract | Recognition of β-glucans by dectin-1 has been shown to mediate cell activation, cytokine production and a variety of antifungal responses. Here, we report that the functional activity of dectin-1 in mucosal immunity to Candida albicans is influenced by the genetic background of the host. Dectin-1 was required for the proper control of gastrointestinal and vaginal candidiasis in C57BL/6 but not BALB/c mice, the latter actually showing increased resistance in the absence of dectin-1. Susceptibility of dectin-1-deficient C57BL/6 mice to infection was associated with defective IL-17A, aryl hydrocarbon receptor-dependent IL-22 production as well as adaptive Th1 responses. In contrast, resistance of dectin-1-deficient BALB/c mice was associated with increased IL-17A and IL-22 production, and the skewing towards Th1/Treg immune responses that provide immunological memory. Disparate canonical/noncanonical NF-κB signaling pathways downstream dectin-1were activated in the two different mouse strains. Thus, the net activity of dectin-1 in antifungal mucosal immunity is dependent on the host’s genetic background that affects both the innate cytokine production as well as the adaptive Th1/Th17 cell activation upon dectin-1 signaling. | por |
dc.description.sponsorship | The studies were supported by the Specific Targeted Research Project “ALLFUN” (FP7−HEALTH−2009 contract number 260338 to LR) and the Italian Project AIDS 2010 by ISS (Istituto Superiore di Sanità - contract number 40H40 to LR) and Fondazione Cassa di Risparmio di Perugia Project n. 2011.0124.021. AC and CC were financially supported by fellowships from Fundação para a Ciência e Tecnologia, Portugal (contracts SFRH/BPD/46292/2008 and SFRH/BD/65962/2009, respectively). | por |
dc.language.iso | eng | por |
dc.publisher | Nature Publishing Group | por |
dc.relation | info:eu-repo/grantAgreement/EC/FP7/260338 | por |
dc.rights | openAccess | por |
dc.subject | Dectin-1 | por |
dc.subject | Mucosal candidiasis | por |
dc.subject | Th1/Th17 | por |
dc.subject | II-22 | por |
dc.subject | genetic background | por |
dc.subject | Mucosal candidiasis, Th1/Th17, Il-22, genetic background | por |
dc.title | Dectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis | por |
dc.type | article | por |
dc.peerreviewed | yes | por |
dc.relation.publisherversion | http://dx.doi.org/10.1038/cmi.2012.1 | por |
sdum.publicationstatus | published | por |
oaire.citationStartPage | 276 | por |
oaire.citationEndPage | 286 | por |
oaire.citationIssue | 3 | por |
oaire.citationTitle | Cellular and Molecular Immunology | por |
oaire.citationVolume | 9 | por |
dc.identifier.doi | 10.1038/cmi.2012.1 | - |
dc.identifier.pmid | 22543832 | por |
dc.subject.wos | Science & Technology | por |
sdum.journal | Cellular and Molecular Immunology | por |
Aparece nas coleções: | ICVS - Artigos em revistas internacionais / Papers in international journals |
Ficheiros deste registo:
Ficheiro | Descrição | Tamanho | Formato | |
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Carvalho A_Cell Mol Immunol 2012 prep.pdf | Versão Preprint | 191,25 kB | Adobe PDF | Ver/Abrir |