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. 2011 Jan 4;121(2):554–568. doi: 10.1172/JCI43984

Figure 2. IL-17 mediates vaccine immunity against B. dermatitidis infection.

Figure 2

(A) Antibody neutralization of IL-17 in vaccinated mice after infection. Lung CFU are the mean ± SEM (n = 10–12). Numbers shown are the relative increase in lung CFU of mAb-treated versus rat IgG controls. *P < 0.001 versus vaccinated mice treated with rat IgG. (B) Neutralization of IL-17 by soluble IL-17 receptor (IL-17R:Fc). Values are the mean ± SEM (n = 10–18); representative of 2 experiments. Numbers shown are the fold increase in lung CFU versus AdLuc-treated controls. *P < 0.001 versus vaccinated mice not treated with adenovirus; **P < 0.001 versus vaccinated mice treated with AdLuc. (C) Lung transcripts and number of primed Th1 and Th17 cells recruited to the lung upon fungal challenge in Il17a–/– and Il17ra–/– mice. RNA from lung (middle panel) and the absolute number of IL-17–, IFN-γ–, or IL-13–producing CD4+CD44+ T cells were quantified by real-time PCR and FACS. Data are mean ± SEM (n = 4–6); representative of 2 experiments. *P < 0.05 versus unvaccinated controls; **P < 0.05 versus vaccinated wild-type and Il17ra–/– mice (D) IL-17RA is required for vaccine immunity. Mean ± SEM (n = 8–12); representative of 2 experiments. *P < 0.001 versus vaccinated wild-type. (E) IL-17A is required for vaccine immunity. Lung CFU are the mean ± SEM (n = 10–12); representative of 2 experiments. Numbers shown in D and E are the fold increase in CFU versus corresponding wild-type controls. *P < 0.001 versus wild-type mice.