Figure 4.

Induction of IL-17A production during C. neoformans strain H99γ infection requires signaling through the IL-17A receptor. BALB/c (white bars) and IL-17RA KO (gray bars) mice were given an intranasal inoculation with C. neoformans strain H99γ. Lungs were excised at day 7 post-inoculation, and pulmonary cytokine production quantified (A) and intracellular IL-17A production was determined in leukocyte populations (B). The lungs were excised at day 7 post-inoculation and a single cell suspension generated using enzymatic digestion. The leukocytes were stained with anti-mouse antibodies (CD45, 1A8 (Neut), CD4, CD8, F4/80 (Mac), CD11b/CD11c (DC), CD4/Fox3p (Treg), CD3/NKp46 (NKT), NKp46/CD45 (NK), γδ/CD45 (γδ+ T cells), CD19 (B cell), SiglecF/CD11b (Eosinophil), fixed, permeabilized, and incubated with anti-mouse antibodies specific for IL-17A and quantified by flow cytometry. Asterisks (*) indicate where significant differences (P < 0.05) were observed between WT and IL-17RA KO mice infected with C. neoformans strain H99γ. Data are cumulative of three experiments using 3 mice per group.

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