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From the Departamento de Biologia Celular e Molecular e Bioagentes Patogênicos,* Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brazil; the Departamento de Imunoparasitologia, Universidade Federal de Uberlândia-ICBIM, Uberlândia, Brazil; the Department of Dermatology, School of Medicine, University of California-Davis, Sacramento, California; and the Laboratório de Oncologia Experimental, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil
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.
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