In a model of pneumococcal meningitis, the TLR2/TLR4 heterodimer regulates inflammatory and antibacterial mechanisms; in mice lacking both TLR2 and TLR4 inoculated intracerebroventricularly with Streptococcus pneumoniae, disease severity is increased, survival is significantly impaired, and the proinflammatory cytokines IL-1β, TNF-α, and IL-6 are decreased, while IFN-γ increases and might lead to long-term neurological problems [141]. This evidence concerns the gene TLR2 and pneumococcal meningitis.