Untangling galectin-driven regulatory circuits in autoimmune inflammation

Abstract

Although significant progress has been made in understanding the mechanisms implicated in the pathogenesis and resolution of autoimmune inflammation, studies aimed at identifying mediators of these pathways are necessary for developing more selective therapies. Galectins, a family of glycan-binding proteins, play central roles in immune cell homeostasis. Whereas some members of this family trigger regulatory programs that promote resolution of inflammation, others contribute to perpetuate autoimmune processes. Here we discuss the roles of endogenous galectins and their specific glycosylated ligands in shaping autoimmune responses by fueling, extinguishing or re-wiring immune circuits. Understanding the relevance of galectin-glycan interactions in autoimmune inflammation could help uncover novel pathways of tolerance breakdown, define molecular signatures for patient stratification and therapy responses and open new avenues for immune intervention.