"Galectin-1 as a selective killer of T cells: implications in immunoregulation in health and disease"

GABRIEL A. RABINOVICH

Jean Les Pins, Francia

Conferencia; Advances in Targeted Therapies 2005; 2005

EULAR, Academia Europea de Reumatología

GALECTINS AND THEIR LIGANDS: AMPLIFIERS, SILENCERS OR TUNERS OF THE INFLAMMATORY RESPONSE?   Gabriel A. Rabinovich Division of Immunogenetics. School of Medicine. University of Buenos Aires E-mail: gabyrabi@ciudad.com.ar   Recent evidence has implicated galectins and their ligands as master regulators of immune cell homeostasis. Whereas some members of this family, such as galectin-3 behave as amplifiers of the inflammatory response, others, such as galectin-1, trigger homeostatic signals to shut off T-cell effector functions. These carbohydrate-binding proteins, identified by shared consensus amino acid sequences and affinity for  b-galactoside-containing sugars, participate in the homeostasis of the inflammatory response, either by regulating cell survival and signaling, influencing cell growth and chemotaxis and interfering with cytokine secretion. Furthermore, recent evidence indicates that galectin-1 might function as a soluble mediator employed by tumour cells to escape immune surveillance. The current wealth of new information promises a future scenario in which individual members of the galectin family or their specific ligands will be used as powerful anti-inflammatory mediators and selective modulators of the immune response.   References 1. Rabinovich GA, Baum LG, Tinari N, Paganelli R, Natoli C, Liu FT & Iacobelli S. Trends Immunol. 2002; 23: 313-320. 3. Rubinstein N, Alvarez M, Zwirner N, Toscano MA, Ilarregui JM, Bravo I, Mordoh J, Fainboim L, Podhajcer O & Rabinovich G. Cancer Cell 2004; 5:241-251. 3. Leffler H, Carlsson S, Hedlund M, Qian Y, Poirier F. Glycoconj. J. 2004; 19:433-440. 4. Rabinovich GA, Daly G, Dreja H, Tailor H, Riera CM, Hirabayashi J, Chernajovsky Y. J. Exp. Med. 1999; 190:385-398. 5. Liu F.-T. & Rabinovich GA. Galectins as modulators of tumour progression. Nat. Rev. Cancer 2005; 5:29-