Our Research Lines

The interpretation of glyco-codes underlying carbohydrate–galectin interactions, particularly Galectin-1 (Gal1), is a key principle for maintaining homeostasis, promoting the resolution of inflammation, and preventing autoimmune phenomena. Our laboratory has demonstrated that Gal1 acts as an immune checkpoint, shaping the fate of myeloid and lymphoid cells. Its administration, through gene or protein therapy, has been shown in preclinical models to mitigate the clinical manifestations of autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, and uveitis, as well as to prevent the development of age-associated inflammation, positioning Gal1 as a promising therapeutic target.

Building on this foundation, our current research focuses on chronic and autoimmune inflammation of the skin, nervous system, and intestine. In these contexts, we map lectin–glycan circuits to understand the mechanisms through which immune balance is disrupted, identify biomarkers and actionable targets, and design therapies aimed at preventing, reversing, or controlling inflammatory processes.

We focus particularly on inflammatory bowel disease (ulcerative colitis and Crohn's disease), multiple sclerosis, and psoriasis. We have demonstrated that Gal1 controls intestinal inflammation in experimental models and are advancing a Gal1 delivery platform designed to enhance local efficacy, reduce adverse effects, enable combinations with existing treatments, and pave the way toward preclinical and clinical validation. At the physiological level, we have also studied these interactions at the maternal–fetal interface.

Our goal is to provide meaningful solutions for individuals whose lives are profoundly affected by these chronic diseases, seeking to mitigate clinical processes, improve patient quality of life, and contribute to a more efficient use of healthcare system resources.