Journal
CELL HOST & MICROBE
Volume 23, Issue 4, Pages 511-+Publisher
CELL PRESS
DOI: 10.1016/j.chom.2018.02.011
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Funding
- Burroughs Wellcome Fund [133-AAB4476]
- NIAID [T32AI007635]
- NHLBI [T32HL007899]
- American Heart Association [17POST32790004]
- USPHS [AI035681]
- Carbone Cancer Center [P30 CA014520]
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Lung epithelial cells (LECs) are strategically positioned in the airway mucosa to provide barrier defense. LECs also express pattern recognition receptors and a myriad of immune genes, but their role in immunity is often concealed by the activities of professional immune cells, particularly in the context of fungal infection. Here, we demonstrate that NF-kappa B signaling in LECs is essential for immunity against the pulmonary fungal pathogen Blastomyces dermatitidis. LECs orchestrate innate antifungal immunity by augmenting the numbers of interleukin-17A (IL-17A)- and granulocyte-macrophage colony-stimulating factor (GM-CSF)-producing innate lymphocytes, specifically natural Th17 (nTh17) cells. Innate lymphocyte-derived IL-17A and GM-CSF in turn enable phagocyte-driven fungal killing. LECs regulate the numbers of nTh17 cells via the production of chemokines such as CCL20, a process dependent on IL-1 alpha-IL-1 receptor (IL-1R) signaling on LECs. Therefore, LECs orchestrate IL-17A- and GM-CSF-mediated immunity in an IL-1R-dependent manner and represent an essential component of innate immunity to pulmonary fungal pathogens.
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