Lack of galectin-3 modifes diferentially Notch ligands in bone marrow and spleen stromal cells interfering with B cell diferentiation
Nenhuma Miniatura disponível
Data
2018
Título da Revista
ISSN da Revista
Título de Volume
Editor
Resumo
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 diferentiation 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 diferentiation in the bone marrow (BM) and spleen. The BM of gal-3-defcient
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
signifcantly increased in the BM and blood of Lgals3−/− mice. For the frst time, we demonstrated that
gal-3 inhibits Notch signaling activation in lymphoid organs regulating earlier and terminal events of B
cell diferentiation.
Descrição
Palavras-chave
Citação
OLIVEIRA, Felipe Leite de et al. Lack of galectin-3 modifies differentially Notch ligands in bone marrow and spleen stromal cells interfering with B cell differentiation. Scientific Reports, London, v. 8, e3495, 2018. DOI: 10.1038/s41598-018-21409-7. Disponível em: https://www.nature.com/articles/s41598-018-21409-7. Acesso em: 21 jan. 2025.