CONICET | Buscador de Institutos y Recursos Humanos

During the past years, galectins, a family of glycan-binding proteins, have been implicated in several biological processes as regulators of the immune system. Particularly, galectin-1 (Gal1) has been shown to play a critical role in the homeostasis of the immune response being able to suppress the clinical manifestations in different experimental models of chronic inflammation and autoimmunity. Based on this background, we studied the function of Gal1 and its specific glycans in the development of the effectors and regulatory B cells. We found that B cells secrete Gal1, particularly in response to LPS and that these cells present a glycosylation signature which is more permissive for Gal1 binding. We also found that B cells from mice deficient in Gal1 (Lgals1-/-) have higher number and frequency of B220+ cells in the spleen than WT mice. However, we could find no significant differences in the transitional 1, transitional 2, marginal zone B cells, follicular B cells and B10 subpopulations. When we studied B cell responses in vitro we found that, although Lgals1-/- and WT B cells have similar activation markers, Lgals1-/- B cells showed reduced proliferation in response to different stimuli. In addition, IL-10 secretion in response to LPS was lower in Lgals1-/- than in WT B cells. Finally, we determined the regulatory properties of galectin-1 on a particular subpopulation of B cells (T2-MZ). We found that, while WT T2- MZ B cells successfully suppressed the proliferation of T cells, Lgals1-/- T2-MZ B cells were unable to generate a T cell inhibitory effect. These results indicate that galectin-1 plays different roles in B cell physiology, being particularly relevant in the regulation of proliferation and the control of regulatory properties.