Suppression of age-related salivary gland autoimmunity by glycosylation-dependent galectin-1-driven immune inhibitory circuits

Abstract

Significance Different immune inhibitory circuits act in concert to prevent and limit the extent of deleterious autoimmune reactions occurring during the aging process. An in-depth understanding of these pathways is critical for implementation of more selective and powerful immunomodulatory modalities capable of attenuating autoimmune inflammation. Here we show that lack of galectin-1 (an endogenous β-galactoside-binding protein) or specific N-glycosylated ligands leads to a gradual breakdown of tolerogenic programs and to the establishment of age-related salivary gland autoimmunity. This study emphasizes the role of lectin–glycan interactions in the maintenance and restoration of immune tolerance and highlights their clinical relevance and therapeutic potential in chronic inflammatory disorders.