| First Author | Bernardes ES | Year | 2006 |
| Journal | Am J Pathol | Volume | 168 |
| Issue | 6 | Pages | 1910-20 |
| PubMed ID | 16723706 | Mgi Jnum | J:109126 |
| Mgi Id | MGI:3625798 | Doi | 10.2353/ajpath.2006.050636 |
| Citation | Bernardes ES, et al. (2006) Toxoplasma gondii infection reveals a novel regulatory role for galectin-3 in the interface of innate and adaptive immunity. Am J Pathol 168(6):1910-20 |
| abstractText | 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. |
