Hence, it is conceivable that the early recognition of S. pneumoniae and, thereby, the initial inflammatory response in the airways at least in part are mediated by TLR2, through an interaction between this receptor and the various TLR2 ligands expressed by the pneumococcus (Yoshimura et al., 1999; Han et al., 2003; Schroder et al., 2003), but that, during a more established infection with a higher bacterial burden, the TLR2-induced inflammation is ‘overruled’ by other pathways stimulated by TLR2-independent pneumococcal antigens. The gene discussed is TLR2; the disease is infection.