Influenza A virus (IAV) infection predisposes individuals to severe infections with bacteria such as Streptococcus pneumoniae (S.p.). Research shows that influenza infection impairs the T helper 17 (Th17) immune response, which is critical in the clearance of S.p. infections. Studies have demonstrated a role for type I Interferons in the impaired Th17 immunity associated with IAV. The results presented in this thesis demonstrate that IAV infection significantly impairs S.p. driven innate and adaptive cytokines. However, this inhibition occurred in the absence of type I Interferons, suggesting an additional mechanism of Th17 immunomodulation associated with IAV. To establish how IAV inhibits these responses, we investigated the effect of IAV infection on specific innate immune Toll Like Receptors (TLRs), which are triggered by S.p. infection. We have identified that IAV targets TLRs (TLR2, TLR4, TLR9) in human monocytes, resulting in a reduction in TLR-induced cytokines. The effect of IAV is more profound on the TLR2 and TLR9 pathways. We established IAV may be inhibiting the TLR9 pathway by targeting RORC, a Th17-specific transcription factor. We investigated if TLR5 agonism could restore IAV-inhibited immune responses. Levels of pneumococcus driven cytokines, which had previously been inhibited by IAV were not reduced in the presence of the TLR5 agonist, suggesting this may restore immune responses despite IAV inhibition. Finally, we sought to investigate the role of the influenza surface glycoprotein, haemagglutinin (HA) in innate and adaptive responses to S.p. and innate responses to TLR agonism. Pneumococcus driven innate and adaptive cytokines were significantly inhibited by HA, whilst certain TLR agonist driven cytokines were also inhibited by HA. Novel findings include determining that immune inhibition by IAV is not solely due to type I IFNs, and demonstrating that TLR5 agonism may be beneficial in circumventing immune inhibition by IAV and restoring Th17 responses.