Surface β-glucans exposed on C. albicans significantly enhance CARD9-mediated proinflammation responses against systemic candidiasis. (A and B) Infected mice survival and kidney CFU assay. Groups of C57B/L6 female mice were injected via lateral tail vein with 1 × 10⁶ CFU of C. albicans WT (CAF2-1), mnn5 mutant, and its restored strain (mnn5/MNN5) in 200 µl sterile saline. Survival of these mice (n = 10 per group) was monitored and plotted (A). Kidney CFU assay (n = 5 per group) was performed at day 2 after infection (B). Shown are means and SD for n = 3. (C and D) WT (Card9^+/+; squares) and CARD9-deficient mice (Card9^−/−; triangles) were infected intravenously with 3 × 10⁵ CFU of C. albicans WT (CAF2-1) and mnn5 mutant strains in 200 µl sterile saline. Survival of these mice (n = 10 per group) was monitored and plotted (C). Kidney CFU assay (n = 5 per group) was performed at day 2 after infection (D). Shown are means and SD for n = 3. (E) ELISA results for TNF, IL-6, IL-1β, and IL-12p40 in mouse sera at day 2 after infection. WT (Card9^+/+) and CARD9-deficient (Card9^−/−) mice (n = 5 per group) were challenged with UV-inactivated C. albicans WT (CAF2-1) and mnn5 mutant yeast cells (1 × 10⁶) in 200 µl sterile saline. Data shown are representative of three independent experiments. SDs are indicated. (F and G) Infected mice survival and kidney CFU assay. Groups of C57B/L6 female mice infected with 6 × 10⁴ CFU of C. albicans WT (CAF2-1) and mnn5 mutant strains, which were treated with 200 µg anti–Dectin-2 monoclonal antibodies (α-D2) or nonspecific control IgG per mouse for four times at 6 h before or 2, 4, or 6 d after injection of C. albicans. Survival of these mice (n = 10 per group) was monitored and plotted (F). Kidney CFU assay (n = 5 per group) was performed at day 2 after infection (G). Shown are means and SD for n = 5. Two independent experiments were conducted (n = 10 in each group). *, P < 0.05; **, P < 0.01; ***, P < 0.001.