Fig. 6: Clec2d knockout mice are highly resistant to infection with C. albicans through increasing IL-12 production. | Nature Communications

Fig. 6: Clec2d knockout mice are highly resistant to infection with C. albicans through increasing IL-12 production.

From: C-type lectin receptor 2d forms homodimers and heterodimers with TLR2 to negatively regulate IRF5-mediated antifungal immunity

Fig. 6

a–c Survival (a), fungal burden in kidney and brain on Day 2 (b), representative histological images with hematoxylin-eosin (H&E) and Periodic Acid-Schiff (PAS) staining of kidney at Day 2 (c) of wild-type and Clec2d-deficient mice intravenously infected with C. albicans (SC5314, 2 × 105 CFU). Scar bars = 20 μm. Arrows indicate fungi hyphae. d–f ELISA of IL-12p70, IFN-γ, IL-12p40 (d), flow assay of frequency and numbers of NK cells (e) and numbers of IFN-γ+ NK cells (f) in kidneys of wild-type and Clec2d-deficient mice after infection with C. albicans for indicated time. g, h Fungal burden in kidneys on Day 2 and brains on Day 1 (g), ELISA of IFN-γ and IL-6 in kidneys on Day 1 (h) of C. albicans-infected wild-type and Clec2d-deficient mice receiving IL-12 neutralizing antibody (αIL-12, 250μg/mouse) or control IgG. i Fungal burden in kidneys and brains on Day 2 of C. albicans-infected wild-type and Clec2d-deficient mice administrated with NK1.1 neutralizing antibody (αNK1.1350 μg/mouse) or control IgG. ns, no significance. Data were presented as mean ± SEM; n = 11(a), n = 3 (e day0 group), n = 4 (d IL-12p70 on Day 0 group), n = 5 (b, d–i) biologically independent samples. Data were analyzed by one-way ANOVA adjusted for multiple comparisons in (b), (d–i), Log-rank Mantel-Cox test in (a). Source data are provided as a Source Data file.

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