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Glycoscience has revealed the key role of glycans or sugars in our cells, providing new therapeutic opportunities. Sugars on the cell surface encode key information that determines their fate and function. The proteins that decode this information, through their interaction with these sugars (ligands), are called lectins. In particular, galectins are those that bind to N-acetyl lactosamine units. When the interaction between lectins and sugars is deregulated, it can influence immunological processes, leading to the development of diseases.

Galectin-1

The research lead by Dr. Gabriel Rabinovich since the 1990s has shown that Galectin-1 (Gal-1), a member of the galectin family, modulates the immune response through its interaction with cellular receptor glycans, acting as immune checkpoints (glycocheckpoints). Gal-1 regulates key mechanisms in cancer and autoimmunity, emerging as a potential therapeutic target in these diseases.

In cancer, tumour cells secrete high levels of Gal-1 into the tumour microenvironment, inducing apoptosis of activated T lymphocytes and polarising dendritic cells and macrophages towards a tolerogenic and immunosuppressive profile, contributing to tumour escape. Gal-1 also promotes tumour neovascularisation through its interaction with vascular endothelial growth factor receptor - type 2 (VEGFR2), inducing resistance of different tumour types to anti-angiogenic therapies, particularly those involving bevacizumab (anti-VEGF monoclonal antibody). To counteract these pro-tumour actions, we developed Gal-1 blocking monoclonal antibodies capable of stimulating the immune response in cancer and preventing neovascularisation phenomena.

On the other hand, in autoimmune (e.g. multiple sclerosis) and chronic inflammatory diseases (e.g. atherosclerosis), where the immune system is exacerbated or unbalanced towards a pro-inflammatory profile, Gal-1 immunosuppressive activity can restore immune homeostasis. To increase the potential of Gal-1 in the inflammatory microenvironment, we have developed Gal-1 variants with enhanced stability and anti-inflammatory capacity.