Lack of galectin-3 up-regulates IgA expression by peritoneal B1 lymphocytes during B cell differentiation

• Published in: Cell and tissue research Vol. 363; no. 2; pp. 411 - 426
• Main Authors: Oliveira, Felipe L., Bernardes, Emerson S., Brand, Camila, dos Santos, Sofia N., Cabanel, Mariana P., Arcanjo, Kátia D., Brito, José M., Borojevic, Radovan, Chammas, Roger, El-Cheikh, Márcia C.
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.02.2016; Springer; Springer Nature B.V
• Subjects: Analysis; Animals; B cells; B-Lymphocytes - cytology; B-Lymphocytes - metabolism; Biomedical and Life Sciences; Biomedicine; Bone morphogenetic proteins; Cell Count; Cell Degranulation; Cell Differentiation; Cell division; Cell Proliferation; Cell Shape; Chronic Disease; Cytokines; Galectin 3 - deficiency; Galectin 3 - metabolism; Growth factors; Human Genetics; Immunoglobulin A; Immunoglobulin A - blood; Immunoglobulin A - metabolism; Immunoglobulin Class Switching; Immunoglobulin M - blood; Interleukin-5; Lymphocytes; Mast Cells - physiology; Mesentery - metabolism; Mice, Inbred C57BL; Molecular Medicine; Omentum - metabolism; Peritoneum - cytology; Phenotype; Plasma; Plasma Cells - metabolism; Protein binding; Proteomics; Regular Article; Schistosoma; Schistosomiasis - blood; Schistosomiasis - immunology; Schistosomiasis - parasitology; Schistosomiasis - pathology; Transforming Growth Factor beta1 - metabolism; Transforming growth factors; Up-Regulation; IgA; Mouse; B lymphocytes; Peritoneal cavity; Plasma cells; Mast cells; Galectin-3; Schistosoma mansoni
• ISSN: 0302-766X; 1432-0878
• DOI: 10.1007/s00441-015-2203-y

Galectin-3 is a β-galactoside-binding protein with an inhibitory role in B cell differentiation into plasma cells in distinct lymphoid tissues. We use a model of chronic schistosomiasis, a well-characterized experimental disease hallmarked by polyclonal B cell activation, in order to investigate the role of galectin-3 in controlling IgA production through peritoneal B1 cells. Chronically infected, galectin-3-deficient mice (Lgals3 ⁻/⁻) display peritoneal fluid hypercellularity, increased numbers of atypical peritoneal IgM⁺/IgA⁺ B1a and B1b lymphocytes and histological disturbances in plasma cell niches when compared with Lgals3 ⁺/⁺ mice. Similar to our infection model, peritoneal B1 cells from uninfected Lgals3 ⁻/⁻ mice show enhanced switching to IgA after in vitro treatment with interleukin-5 plus transforming growth factor-β (IL-5 + TGF-β1). A higher number of IgA⁺ B1a lymphocytes was found in the peritoneal cavity of Lgals3 ⁻/⁻-uninfected mice at 1 week after i.p. injection of IL-5 + TGF-β1; this correlates with the increased levels of secreted IgA detected in the peritoneal fluid of these mice after cytokine treatment. Interestingly, a higher number of degranulated mast cells is present in the peritoneal cavity of uninfected and Schistosoma mansoni-infected Lgals3 ⁻/⁻ mice, indicating that, at least in part, mast cells account for the enhanced differentiation of B1 into IgA-producing B cells found in the absence of galectin-3. Thus, a novel role is revealed for galectin-3 in controlling the expression of surface IgA by peritoneal B1 lymphocytes; this might have important implications for manipulating the mucosal immune response.