IL-17A promotes expression of cytotoxic-mediator genes independently of CD4+ T cells. (A to D) Seven- to 9-week-old WT (C57BL/6J) and Il17a−/− mice (n = 6 mice/group) were infected (i.p.) with 100 PFU of WNV and sacrificed at 8 dpi to isolate splenocytes and CD8+ T cells. Splenocytes or CD4+ T cell-depleted splenocytes (CD4− splenocytes) were cultured with or without recombinant mouse IL-17A (rIL17A) (50 ng/ml) for 24 h ex vivo, and RFC of transcripts of perforin-1 (A), granzyme A (B), granzyme B (C), and FasL (D) was measured by qPCR (normalized to cellular β-actin mRNA). (E and F) Splenocytes (E) or purified CD8+ T cells (F) were cultured ex vivo with or without recombinant IL-17A (50 ng/ml) for 24 h, and expression (RFC) of Act-1 was by measured qPCR. (G) RFC of indicated genes in splenocytes cultured ex vivo for 24 h with or without rIL17A (50 ng/ml) in the presence of Bay-11-7082 (4 μM) or dimethyl sulfoxide (DMSO) as a vehicle control (<0.05%). All the data (means and SEM) represent the results of two independent experiments (n = 3 mice/group) compared by two-tailed Student t tests. (A to F) All the data from WT and Il17a−/− mice were normalized to the respective mock-treated controls. *, P < 0.05; **, P < 0.005; ns, not significant (P > 0.05).