Dectin-1/IL-15 Pathway Affords Protection against Extrapulmonary <i>Aspergillus fumigatus</i> Infection by Regulating Natural Killer Cell Survival

Author:

Yoshikawa Fábio S.Y.ORCID,Wakatsuki Maki,Yoshida Kosuke,Yabe Rikio,Torigoe Shota,Yamasaki Sho,Barber Glen N.,Saijo Shinobu

Abstract

<i>Aspergillus fumigatus</i> is a ubiquitous, yet potentially pathogenic, mold. The immune system employs innate receptors, such as dectin-1, to recognize fungal pathogens, but the immunological networks that afford protection are poorly explored. Here, we investigated the role of dectin-1 in anti-<i>A. fumigatus</i> response in an experimental model of acute invasive aspergillosis. Mice lacking dectin-1 presented enhanced signs of inflammation, with increased production of inflammatory cytokines and neutrophil infiltration, quickly succumbing to the infection. Curiously, resistance did not require T/B lymphocytes or IL-17. Instead, the main effector function of dectin-1 was the preservation of the NK cell population in the kidneys by the provision of the cytokine IL-15. While the depletion of NK cells impaired host defense in wild-type mice, IL-15 administration restored antifungal responses in dectin-1-deficient mice. Our results uncover a new effector mechanism for dectin-1 in anti-<i>Aspergillus</i> defense, adding an alternative approach to understand the pathophysiology of this infection.

Publisher

S. Karger AG

Subject

Immunology and Allergy

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