After infection with the ME-49 strain of T. gondii, Gal-3-/- mice exhibited a higher parasite burden, decreased recruitment of monocytes/macrophages and neutrophils, delayed inflammatory response in the central nervous system and significantly showed higher concentrations of IL12 and IFNγ in serum compared to Gal-3+/+ mice, suggesting that Gal-3 is an important molecule in the course of an immune response to control T. gondii proliferation in vivo (Bernardes et al., 2006). Here, IFNG is linked to infection.