Abstract
Galectin-1 (Gal-1), a member of a family of highly conserved carbohydrate-binding proteins, has been reported to be a potent immunosuppressive and anti-inflammatory factor. It has been proposed that the presence of galectin-1 in organs such as the eye, the placenta, reproductive organs (testis, ovaries) and also in tumours might confer a status of immune privilege to these vulnerable sites. Up-regulated expression of this protein may contribute to preserve an immunosuppressive microenvironment by inducing apoptosis of inflammatory and effector T cells and skewing the balance of the local immune response towards a Th2 cytokine profile. Different glycosyltransferase enzymes are involved in the generation of specific saccharide ligands required for Gal-1 binding and Gal-1-induced cell death. Interestingly, expression of these enzymes is highly regulated during T cell development, activation and apoptosis. The aim of this review is to explore the potential link between glycosylation of immune cell subsets, susceptibility to Gal-1 and the generation of immune privilege, particularly in the context of tumor-immune escape.
