The correlation between late, but not early, expression and production of IL-10 in E. muris/ nonlethally infected mice and IOE-infected Nod2-/- mice and survival, protective immunity, minimal pathology and high IFN-γ:IL-10 ratio at early and late stages of infection, suggests that IL-10 may control excessive inflammatory responses and thus inhibits immunopathology without negatively affecting IFN-γ mediated bacterial elimination. This evidence concerns the gene NOD2 and infection.