Fig. 4: Deficiency of PD-L1 significantly increases survival of C. albicans-infected mice through promoting neutrophil migration from bone marrow into kidney.
From: PD-L1 negatively regulates antifungal immunity by inhibiting neutrophil release from bone marrow
a Neutrophil tracking assay in the bone marrow and kidney of wild-type and Cd274−/− mice, which were intravenously infection with C. albicans SC5314 (2 × 105 CFU/mouse) for indicated days. PE-labeled anti-CD45 (10 μl) were microinjected into one tibia for 12 h before scarification at each indicated time. b–e The percentage of neutrophils in bone marrow and kidney (b), ELISA quantification of CXCL1 and CXCL2 in bone marrow (c), survival and kidney fungal burden (d), and PAS staining (e) of kidney of wild-type and Cd274−/− mice, which were intravenously infection with C. albicans SC5314 (2 × 105 CFU/mouse) for indicated days. Scar bars = 50 μm. f–i The percentage of Ly-6G+ neutrophils in bone marrow and kidney (f, h) and kidney fungal burden (g, i) of naive and C. albicans (2 × 105 CFU/mouse)-infected wild-type and Cd274−/− mice on day 4, which were pretreated with IgG (Control, 5 or 40 ng/mouse), anti-CXCL1 (αCXCL1, 5 ng/mouse), and anti-CXCL2 (αCXCL2, 40 ng/mouse) into tibia for 12 h before scarification. Data were presented as mean ± SD; n = 5 (b–d, f–i), n = 6 (a), n = 10 (d) biological independent samples. Data were analyzed by unpaired two-sided Student’s t test in a–d, g, i, one-way ANOVA adjusted for multiple comparisons in f, h or two-sided log rank (Mantel–Cox) tests in d. Source data are provided as a Source data file.
