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Dectin- 1 isoforms contribute to distinct Th 1/Th 17 cell activation in mucosal candidiasis

Cellular & Molecular Immunology 2012年第3期9卷 276-286页

作者： Agostinho Carvalho Gloria Giovannini AntoneUa De Luca Carmen D＇Angelo andrea casagrande Rossana G Iannitti Giovanni Ricci Cristina Cunha Luigina Romani Department of Experimental Medicine and Biochemical Sciences University of Perugia Perugia Italy Life and Health Sciences Research Institute （ICVS） School of Health Sciences University of Minho Braga Portugal CVS/3B＇s--PT Government Associate Laboratory Braga/Guimaraes Portugal

The recognition of p-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 C57BIJ6, but not BALB/c mice; in fact, the latter showed increased resistance in the absence of dectin-1. The susceptibility of dectin-l-deficient C57BL/6 mice to infection was associated with defects in IL-17A and aryl hydrocarbon receptor-dependent IL-22 production and in adaptive Th I responses. In contrast, the resistance of dectin- 1-deficient BALB/c mice was associated with increased IL-17A and IL-22 production and the skewing towards Thl/Treg immune responses that provide immunological memory. Disparate canonical/ noncanonical NF-KB signaling pathways downstream of dectin-1 were 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, which affects both the innate cytokine production and the adaptive Th1/Th17 cell activation upon dectin-1 signaling.

关键词： Dectin-1 Mucosal candidiasis, Th1/Th17, 11-22, genetic background

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