Extended Data Fig. 5: The acquired fungal virulence is not explained by aberrant IFN-I, IFN-γ or IL-13 expression.
From: IL-17-mediated antifungal immunity restricts Candida albicans pathogenicity in the oral cavity

Il17rc−/− Ifnar−/−, Il17rc−/− Ifngr−/− or Il17rc−/− Il4ra−/− double knockout mice and the respective heterozygous littermate control mice (Il17rc−/−) were associated with C. albicans strain 101 for 19 days. A. Tongue CFUs (n = 7, 8 or 9 / group, mean ± SEM, data pooled from 2-3 independent experiments). B. PAS-stained tongue sections (representative of at least 7 mice / group from 2-3 independent experiments). Scale bars: 100 μm; 25 μm for the inserts. C.–H. Il22, Krt10, and Dsg4 host transcripts and ECE1, HWP1, and SAP5 fungal transcripts in the colonized tongue as indicated. n = 4, 5, 7, 8 or 9 / group, mean ± SEM, data pooled from 2-3 independent experiments (or, for some genes n = 3 from one representative experiment, mean ± SD). The grey shaded area represents the expression levels of each host gene in naïve animals. The statistical significance of differences between groups was determined by two-sided Mann-Whitney (A, left panel) or two-sided unpaired t-test (A, middle and right panels, and C–H). ns, not significant (p ≥ 0.05).