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TitleDectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis
Author(s)Carvalho, Agostinho
Giovannini, Gloria
De Luca, Antonella
D’Angelo, Carmen
Casagrande, Andrea
Iannitti, Rossana G.
Ricci, Giovanni
Cunha, Cristina
Romani, Luigina
Mucosal candidiasis
genetic background
Mucosal candidiasis, Th1/Th17, Il-22, genetic background
Issue dateMay-2012
PublisherNature Publishing Group
JournalCellular and Molecular Immunology
Abstract(s)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.
DescriptionWe thank Dr. Cristina Massi Benedetti for digital art and editing
Publisher version
AccessOpen access
Appears in Collections:ICVS - Artigos em revistas internacionais / Papers in international journals

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