biostudies-literatureUnknown8(1)de Oliveira FLGalectin-3 (Gal-3) is a β-galactoside binding protein that controls cell-cell and cell-extracellular matrix interactions. In lymphoid organs, gal-3 inhibits B cell differentiation by mechanisms poorly understood. The B cell development is dependent on tissue organization and stromal cell signaling, including IL-7 and Notch pathways. Here, we investigate possible mechanisms that gal-3 interferes during B lymphocyte differentiation in the bone marrow (BM) and spleen. The BM of gal-3-deficient mice (Lgals3^-/- mice) was evidenced by elevated numbers of B220⁺CD19⁺c-Kit⁺IL-7R⁺ progenitor B cells. In parallel, CD45^- bone marrow stromal cells expressed high levels of mRNA IL-7, Notch ligands (Jagged-1 and Delta-like 4), and transcription factors (Hes-1, Hey-1, Hey-2 and Hey-L). The spleen of Lgals3^-/- mice was hallmarked by marginal zone disorganization, high number of IgM⁺IgD⁺ B cells and CD138⁺ plasma cells, overexpression of Notch ligands (Jagged-1, Delta-like 1 and Delta-like 4) by stromal cells and Hey-1. Morever, IgM⁺IgD⁺ B cells and B220⁺CD138⁺ CXCR4⁺ plasmablasts were significantly increased in the BM and blood of Lgals3^-/- mice. For the first time, we demonstrated that gal-3 inhibits Notch signaling activation in lymphoid organs regulating earlier and terminal events of B cell differentiation.Scientific reports3495https://www.ebi.ac.uk/biostudies/studies/S-EPMC5823902biostudies-literatureLack of galectin-3 modifies differentially Notch ligands in bone marrow and spleen stromal cells interfering with B cell differentiation.PMC5823902Pereira JXFermino MLde Oliveira FLRicon LBrand CEl-Cheikh MCBernardes ESDos Santos SNda Costa TPChammas RfalseLack of galectin-3 modifies differentially Notch ligands in bone marrow and spleen stromal cells interfering with B cell differentiation.Galectin-3 (Gal-3) is a β-galactoside binding protein that controls cell-cell and cell-extracellular matrix interactions. In lymphoid organs, gal-3 inhibits B cell differentiation by mechanisms poorly understood. The B cell development is dependent on tissue organization and stromal cell signaling, including IL-7 and Notch pathways. Here, we investigate possible mechanisms that gal-3 interferes during B lymphocyte differentiation in the bone marrow (BM) and spleen. The BM of gal-3-deficient mice (Lgals3^-/- mice) was evidenced by elevated numbers of B220⁺CD19⁺c-Kit⁺IL-7R⁺ progenitor B cells. In parallel, CD45^- bone marrow stromal cells expressed high levels of mRNA IL-7, Notch ligands (Jagged-1 and Delta-like 4), and transcription factors (Hes-1, Hey-1, Hey-2 and Hey-L). The spleen of Lgals3^-/- mice was hallmarked by marginal zone disorganization, high number of IgM⁺IgD⁺ B cells and CD138⁺ plasma cells, overexpression of Notch ligands (Jagged-1, Delta-like 1 and Delta-like 4) by stromal cells and Hey-1. Morever, IgM⁺IgD⁺ B cells and B220⁺CD138⁺ CXCR4⁺ plasmablasts were significantly increased in the BM and blood of Lgals3^-/- mice. For the first time, we demonstrated that gal-3 inhibits Notch signaling activation in lymphoid organs regulating earlier and terminal events of B cell differentiation.2018-01-01T00:00:00Z2018 Feb2024-11-10T04:17:52.849Z2019-03-26T23:04:01ZS-EPMC58239022947256810.1038/s41598-018-21409-7