In a murine model of pneumococcal meningitis, we found that B7-H3 strongly enhanced S. pneumoniae-stimulated proinflammatory cytokine and chemokine expression in the brain via a TLR2-dependent mechanism, and this B7-H3-amplified inflammatory response further exacerbated S. pneumoniae-induced disruption of blood-brain barrier (BBB) integrity and brain damage [13,23], indicating that B7-H3 participates in the development of pneumococcal meningitis via augmentation of the innate immunity-associated inflammatory response. Here, TLR2 is linked to pneumococcal meningitis.