| First Author | de Oliveira FL | Year | 2018 |
| Journal | Sci Rep | Volume | 8 |
| Issue | 1 | Pages | 3495 |
| PubMed ID | 29472568 | Mgi Jnum | J:262581 |
| Mgi Id | MGI:6163104 | Doi | 10.1038/s41598-018-21409-7 |
| Citation | de Oliveira FL, et al. (2018) Lack of galectin-3 modifies differentially Notch ligands in bone marrow and spleen stromal cells interfering with B cell differentiation. Sci Rep 8(1):3495 |
| abstractText | Galectin-3 (Gal-3) is a beta-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. |
