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Immunity. 2014 Jan 16;40(1):117-27. doi: 10.1016/j.immuni.2013.12.002. Epub 2014 Jan 9.

IL-17 regulates systemic fungal immunity by controlling the functional competence of NK cells.

Author information

1
Institute of Microbiology, ETH Zurich, Vladimir-Prelog-Weg 4, 8093 Zürich, Switzerland.
2
Immunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.
3
Institute of Microbiology, ETH Zurich, Vladimir-Prelog-Weg 4, 8093 Zürich, Switzerland. Electronic address: leibundgut@micro.biol.ethz.ch.

Abstract

Interleukin 17 (IL-17)-mediated immunity plays a key role in protection from fungal infections in mice and man. Here, we confirmed that mice deficient in the IL-17 receptor or lacking the ability to secrete IL-17 are highly susceptible to systemic candidiasis, but we found that temporary blockade of the IL-17 pathway during infection in wild-type mice did not impact fungal control. Rather, mice lacking IL-17 receptor signaling had a cell-intrinsic impairment in the development of functional NK cells, which accounted for the susceptibility of these mice to systemic fungal infection. NK cells promoted antifungal immunity by secreting GM-CSF, necessary for the fungicidal activity of neutrophils. These data reveal that NK cells are crucial for antifungal defense and indicate a role for IL-17 family cytokines in NK cell development. The IL-17-NK cell axis may impact immunity against not only fungi but also bacteria, viruses, and tumors.

PMID:
24412614
DOI:
10.1016/j.immuni.2013.12.002
[Indexed for MEDLINE]
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