Toxoplasma gondii Infection Reveals a Novel Regulatory Role for Galectin-3 in the Interface of Innate and Adaptive Immunity

• DOI: 10.2353/ajpath.2006.050636
• Publication Date: 2006-08-21T21:17:32Z
• Authors: Emerson Soares Be...; Neide M. Silva; Luciana Pereira Ruas; Jose Roberto Mineo; Adriano Motta Loyola; Daniel K. Hsu; Fu-Tong Liu; Roger Chammas; Maria Cristina Ro...
• Keywords: Galectin 3; Mice, Transgenic; Dendritic Cells; Interleukin-12; Immunity, Innate; CD11c Antigen; Up-Regulation; 3. Good health; Mice, Inbred C57BL; Mice; 03 medical and health sciences; Toxoplasmosis, Animal; 0302 clinical medicine; Immune System; Animals; Toxoplasma; Spleen; Toxoplasmosis

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 pro-inflammatory effect but also a regulatory role on dendritic cells, capable of interfering in the adaptive immune response.