Regulated expression of galectin-1 during B-cell activation and implications for T-cell apoptosis.

Galectin-1 (GAL-1), a highly conserved beta-galactoside-binding protein, has shown immunomodulatory properties. In this study, we investigated the regulation of GAL-1 expression within the B-cell compartment using Trypanosoma cruzi infection as a natural model of in vivo B-cell activation. GAL-1 was found to be expressed on activated B cells from T. cruzi-infected mice, mainly localized at the cytosolic compartment. Expression of this protein was found to be modulated according to the activation state of the cells, revealing a significant increase in stimulated B cells that received signals via cross-linking of the B-cell receptor and CD40. It was found that GAL-1 was secreted by B cells to the extracellular milieu upon activation. Finally, purified GAL-1 produced by activated B cells induced apoptosis of T cells but not B cells and also influenced interferon-gamma cytokine production. Hence, the present study describes a potential mechanism by which B cells can regulate T-cell function and survival.