Gabriel Rabinovich is a biochemist recognized for his contributions to emerging areas at the frontiers of immunology, glycobiology and tumor biology. His work builds on the identification of the immunoregulatory functions of galectins, an evolutionarily-conserved family of endogenous glycan-binding proteins. Among his most prominent findings, Rabinovich discovered that galectin-glycan interactions were critical components of a central regulatory checkpoint that reduces excessive inflammation and prevents autoimmune pathology, while at the same time fostering immune privilege and promoting angiogenesis in cancer. Rabinovich was born in Córdoba, Argentina in 1969 and obtained his first degree in Biochemistry and his Ph.D. from the School of Chemical Sciences at the National University of Córdoba. He has mentored numerous Ph.D. and post-doctoral fellows, served on the editorial board of several journals, held visiting professorships at international universities and is member of the US National Academy of Sciences, the Third World Academy of Sciences and the Argentinean Academy of Sciences. He is Senior Investigator of the National Research Council (CONICET) and Professor of Immunology at the School of Exact and Natural Sciences, University of Buenos Aires. He currently heads the Division of Immunopathology at the Institute of Biology and Experimental Medicine (IBYME) and is Deputy Director of IBYME.

Research Interests

Gabriel Rabinovich's laboratory is interested in understanding the function of glycans and glycan-binding proteins in cellular processes relevant to immune regulation, tolerance and angiogenesis in health and disease. Using an interdisciplinary approach, they have demonstrated that endogenous galectins, a family of soluble glycan-binding proteins, can translate glycan-encoded information into novel regulatory programs that control inflammation, suppress autoimmune pathology and allow cancer cells to evade immune responses and promote blood vessel formation. Together with his team, Rabinovich has demonstrated that galectin-dependent regulatory programs can blunt harmful immune responses by selectively depleting pathogenic T cells, triggering differentiation of tolerogenic dendritic cells and promoting polarization of macrophages and microglia toward an anti-inflammatory phenotype. Moreover, they have identified a dynamically-regulated "glycan signature" on immune cells that acts as an "on-and-off" switch to control the regulatory function of galectins. They demonstrated that malignant cells can use the galectin-glycan pathway to create immunosuppressive networks that thwart antitumor responses. Notably, they found that galectin-glycan interactions can also preserve angiogenesis in tumors refractory to anti-angiogenic treatment by recapitulating the signaling activity of vascular endothelial growth factor. These findings open new possibilities for development of therapeutic strategies aimed at potentiating antitumor responses, limiting autoimmune inflammation and overcoming aberrant angiogenesis.

Membership Type

International Member

Election Year


Primary Section

Section 43: Immunology and Inflammation

Secondary Section

Section 22: Cellular and Developmental Biology