Detalhes bibliográficos
| Resumo: | 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. |
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| Autores principais: | Carvalho, Agostinho |
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| Outros Autores: | Giovannini, Gloria; De Luca, Antonella; D’Angelo, Carmen; Casagrande, Andrea; Iannitti, Rossana G.; Ricci, Giovanni; Cunha, Cristina; Romani, Luigina |
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| Assunto: | Dectin-1 Mucosal candidiasis Th1/Th17 II-22 genetic background Mucosal candidiasis, Th1/Th17, Il-22, genetic background |
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| Ano: | 2012 |
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| País: | Portugal |
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| Tipo de documento: | artigo |
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| Tipo de acesso: | acesso aberto |
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| Instituição associada: | Universidade do Minho |
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| Idioma: | inglês |
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| Origem: | RepositóriUM - Universidade do Minho |
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