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

Emerson Soares Bernardes, Neide M. Silva, Luciana Pereira Ruas, Jose Roberta Mineo, Adriano Motta Loyola, Daniel K. Hsu, Fu-Tong Liu, Roger Chammas, Maria Cristina Roque-Barreira

Research output: Contribution to journalArticle

97 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1910-1920
Number of pages11
JournalAmerican Journal of Pathology
Volume168
Issue number6
DOIs
StatePublished - Jun 2006

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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