Role of Dectin-2 for Host Defense against Systemic Infection with Candida glabrata

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Ifrim, Daniela | Bain, Judith | Reid, Delyth | Oosting, Marije | Verschueren, Ineke | Gow, Neil | van Krieken, J Han | Brown, Gordon, D | Kullberg, Bart-Jan | Joosten, Leo | van Der Meer, Jos, W. M. | Koentgen, Frank | Erwig, Lars | Quintin, Jessica | Netea, Mihai, G.

Edité par CCSD ; American Society for Microbiology -

International audience. 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 decrease in phagocytosis of the fungus by the Dectin-2(-/-) macrophages and neutrophils. Neutrophils of Dectin-2(-/-) mice also displayed 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 into the host defense mechanisms against this important fungal pathogen.

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