Toxoplasma gondii infection reveals a novel regulatory role for galectin-3 in the interface of innate and adaptive immunity

In attempts to investigate the role of galectin-3 in innate immunity, we studied galectin-3-deficient (gal3(-/-)) mice with regard to their response to Toxoplasma gondii infection, which is characterized by inflammation in affected organs, Th-1-polarized immune response, and accumulation of cysts in the central nervous system. in wild-type (gal3(+/+)) mice, infected orally, galectin-3 was highly expressed in the leukocytes infiltrating the intestines, liver, lungs, and brain. Compared with gal3(+/+), infected gal3(-/-) mice developed reduced inflammatory response in all of these organs but the lungs. Brain of gal3(-/-) mice displayed a significantly reduced number of infiltrating monocytes/macrophages and CD8(+) cells and a higher parasite burden. Furthermore, gal3-/- mice mounted a higher Th1-polarized response and had comparable survival rates on peroral T gondii infection, even though they were more susceptible to intraperitoneal infection. Interestingly, splenic cells and purified CD11c(+) dendritic cells from gal3(-/-) mice produced higher amounts of interleukin-12 than cells from gal3(+/+) mice, possibly explaining the higher Th1 response verified in the gal3-/- mice. We conclude that galectin-3 exerts an important role in innate immunity, including not only a proinflammatory effect but also a regulatory role on dendritic cells, capable of interfering in the adaptive immune response.