Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17931 (galectin-3)
 2,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many parasitic helminths produce large quantities of glycosylated proteins, some if which are believed to be involved in the skewing towards the dominant Th2 response observed during helminth infection. Galectin-3 is a member of a family of lectin-binding proteins produced by many different types of immune cells, including macrophages. Galectin-3 recognizes the GalNAcbeta1-4GlcNAc (LDN) epitope present on many helminth antigens, including those of the schistosome eggs. Here we show that galectin-3 is not involved in the development of the Th2 response nor in schistosome granuloma formation. Galectin-3-deficient mice were able to expel the gastrointestinal nematode Trichuris muris at the same speed as wild-type mice. Expulsion of T. muris is known to be dependent on a Th2 immune response and galectin-3-deficient mice showed no defect in their ability to produce Th2 cytokines or in their antibody responses, compared to wild-type mice. Furthermore, galectin-3-deficient mice were also able to mount a Th2 response to Schistosoma mansoni infection and they exhibited normal hepatic granuloma formation. The data presented here demonstrate that galectin-3 is not a critical component in the development of Th2 responses during helminth infection in vivo, nor is it essential for schistosome egg granuloma formation.
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PMID:Lack of galectin-3 involvement in murine intestinal nematode and schistosome infection. 1724 97

Galectin-3 (Gal-3) is a beta-galactoside binding lectin displaying both intracellular and extracellular immune functions. In Schistosoma mansoni infection, Gal-3 has been associated with the induction of a T helper 2 response. Whereas dendritic cells (DCs) play a pivotal role in the regulation of T cell differentiation, little is known about the regulation of Gal-3 expression in DCs. In this study we determined Gal-3 mRNA and protein levels during in vitro differentiation of human monocytes into immature DCs (iDCs), by culturing monocytes in the presence of interleukin-4 (IL-4) and granulocyte-macrophage colony-stimulating factor (GM-CSF). Gal-3 mRNA levels show a moderate, transient increase during iDC generation, accompanied by elevated cell-associated Gal-3 protein. Our data show that culturing monocytes with IL-4 alone strongly increases Gal-3 mRNA levels, whereas GM-CSF induces a low increase in Gal-3 mRNA. The combined data indicate that GM-CSF reduces IL-4 induced Gal-3 mRNA levels during the generation of iDC. Remarkably, stimulation of monocytes with GM-CSF results in secretion of significant amounts of Gal-3 in the medium, whereas iDCs do not release detectable amounts of Gal-3, indicating a suppressive role of IL-4 on GM-CSF induced Gal-3 secretion. Finally, our data demonstrate that all differentiated cell types tested show a significantly lower capacity to bind Gal-3 on the cell surface than monocytes. In conclusion, Gal-3 expression in iDCs is restricted, and Gal-3 protein is localized mainly intracellular, due to the opposite actions of IL-4 and GM-CSF. By these properties, the DCs may be protected against Gal-3 induced phosphatidylserine (PS) exposure and/or apoptosis.
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PMID:Regulation of expression and secretion of galectin-3 in human monocyte-derived dendritic cells. 1969 26