The role of Dectin-2 for host defense against systemic infection with Candida glabrata

Daniela C. Ifrim, Judith M. Bain, Delyth M. Reid, Marije Oostinga, Ineke Verschueren, Neil A. R. Gow, J. Han van Krieken, Gordon D. Brown, Bart-Jan Kullberg, Leo A B Joosten, Jos W. M. van der Meer, Frank Koentgen, Lars P. Erwig, Jessica Quintin, Mihai G. Netea

Research output: Contribution to journalArticlepeer-review

78 Citations (Scopus)
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Although Candida glabrata is an important pathogenic Candida species, relatively little is known about its innate immune recognition. Here we explore the potential role of Dectin-2 for host defense against C. glabrata. Dectin-2-deficient (Dectin-2-/-) mice were found to be more susceptible to C. glabrata infections, showing a defective fungal clearance in kidneys, but not in the liver. The increased susceptibility to infection was accompanied by lower production of T helper 1 (Th1) and Th17-derived cytokines by splenocytes of Dectin-2-/- mice, while macrophage-derived cytokines were less affected. These defects were associated with a moderate, yet significant, decreased phagocytosis of the fungus by the Dectin-2-/- macrophages and neutrophils. Neutrophils of Dectin-2-/- mice also displayed a lower production of reactive oxygen species (ROS) upon challenge with opsonized C. glabrata or C. albicans. This study suggests that Dectin-2 is important in host defense against C. glabrata and provides new insights in the host defense mechanisms against this important fungal pathogen.
Original languageEnglish
Pages (from-to)1064-1073
Number of pages10
JournalInfection and Immunity
Issue number3
Early online date16 Dec 2013
Publication statusPublished - Mar 2014


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