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. Author manuscript; available in PMC: 2018 Oct 31.
Published in final edited form as: Nat Med. 2016 Jul 18;22(8):915–923. doi: 10.1038/nm.4134

Figure 3. Cblb controls anti-fungal activities of dendritic cells and macrophages.

Figure 3

(a) Killing capacity of BM-neutrophils, BM-M, BM-DC, BM-monocytes, or splenic DC as assessed by co-culture with C. albicans. Assays performed in quadruplicates. (b,c) Killing capacity of BM-DC in the presence of (b) the phagocytosis inhibitor Dynasore or an anti-Dectin-1 antibody, or (c) the SYK inhibitor R406. (d,e) ROS production by intraperitoneal immune infiltrates of Cblb+/+ or CblbΔ/Δ mice 24 h after intraperitoneal C. albicans infection (5 * 106 CFU/21.5 g body weight). Plots depict (d) ROS production by immune infiltrates without re-stimulation or (e) with re-stimulation with C. albicans. Experiments performed in triplicates. (f) Killing capacity of immune infiltrates from (d,e). (g,h) ROS production of (g) monocytes/macrophages or (h) neutrophils FACS sorted from infiltrates in (d,e). (i,j) Cblb+/+ or CblbΔ/Δ mice were injected with PBS liposomes or clodronate liposomes 24 h before and 24 h after intravenous infection with C. albicans (105 CFU/21.5 g body weight) and monitored for (i) weight loss, as compared to starting weight (P values assessed by two-way ANOVA), or (j) survival (P values assessed with log rank test). n = 5 for PBS liposome treated, n = 8 for clodronate liposome treated cohorts. For panels (a-c,f,i) data are shown as means ± standard deviation. For panels (a,b) 1 representative of 5, for panels (c-j) 1 representative of 3 independent experiments is shown. *P < 0.05, **P < 0.01, ***P < 0.001 as calculated with Student’s t-test, unless stated otherwise.