Figure 6.

Neutrophil and γδ+T cell depletion does not affect fungal burden, but does abrogate IL-17A production in mice infected with C. neoformans strain H99γ. BALB/c mice received an intranasal inoculum of 1 × 104 CFU of C. neoformans strain H99γ in 50 μl of sterile PBS. Prior to and during infection, mice were treated with isotype control antibody (white bars) or with anti-1A8 antibody (gray bars), anti-1A8/CD4 (checkered bars), anti-1A8/CD8 (slashed bars), anti-1A8/CD4/CD8 (striped bars), and anti-1A8/γδ (thin slashed bars). Lungs were excised at day 7 post-inoculation, and IL-17A (A) and pulmonary cryptococcal burden (B) quantified. Asterisks (*) indicate where significant increases in depleted mice compared to isotype-control treated mice (P < 0.05), tau (τ) indicates significant decreases in depleted mice compared to neutrophil (1A8) depleted mice (P < 0.05) following infection with C. neoformans strain H99γ. Fungal burden results are expressed as mean CFU per milliliter ± standard errors of the mean (SEM), and IL-17A results are expressed as the mean pg/ml ± SEM. Data are cumulative of three experiments using 4 mice per group.

Wozniak et al. BMC Immunology 2012 13:65   doi:10.1186/1471-2172-13-65
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