In particular, using the murine model of pneumococcal TIGR4 meningitis, we have shown: (i) high expression of IFN-γ in the brain of infected mice, (ii) recruitment in the brain of IFN-γ-producing leukocytes, (iii) protection of mice from lethality by the in vivo IFN-γ antibody-mediated neutralization. Here, IFNG is linked to meningitis.