Previous studies in mice demonstrated that during T. gondii infection, neutrophils are rapidly recruited to the sites of infection and contribute to the production of cytokines and chemokines, such as interleukin-12 (IL-12), interferon gamma (IFN-γ), chemokine (C-C motif) ligand 3 (CCL3) and CCL4, which are protective against T. gondii infection (8, 9). This evidence concerns the gene CCL4 and infection.