We the editors of Cell Host & Microbe have been informed by the Lead Contact and corresponding author of this paper, Dr. Bruce S. Klein, that additional experimentation following the publication of the paper has raised an issue with the results reported in Figure 7H. The paper reported an essential role for lung epithelial cells (LEC) in orchestrating IL-17A- and GM-CSF-mediated immunity to the pulmonary fungal pathogen Blastomyces dermatitidis. In Figure 7H of the paper, the authors tested the role of the chemokine receptor CCR6 in LEC-mediated immunity and reported that CCR6-deficient mice exhibited significantly higher lung fungal burden, supporting a role for the CCL20-CCR6 axis of chemokine signaling in antifungal immunity. After the paper was published, experiments performed with larger numbers of animals revealed that the effect on lung fungal burden in CCR6−/− mice is not statistically significant. While the finding that chemokine receptor signaling is essential remains unchanged, a specific role for CCR6 in the process is no longer supported. With this note, we and the authors would like to alert the community and direct you to additional data related to Figure 7H, which have been deposited in Mendeley Data and can be accessed here. The remaining findings in the paper are unchanged, and the new data do not alter the main conclusions of the paper.
. Author manuscript; available in PMC: 2020 Apr 7.
Published in final edited form as: Cell Host Microbe. 2019 Apr 10;25(4):630. doi: 10.1016/j.chom.2019.03.013