Galectins

Juan P Cerliani, Tomas Dalotto-Moreno, Daniel Compagno, L Sebastián Dergan-Dylon, Diego J Laderach, Lucas Gentilini, Diego O Croci, Santiago P Méndez-Huergo, Marta A Toscano, Mariana Salatino, Gabriel A Rabinovich, Juan P. Cerliani, L. Sebastián Dergan-Dylon, Diego J. Laderach, Diego O. Croci, Santiago P. Méndez-Huergo, Marta A. Toscano, Gabriel A. Rabinovich

During the past decade, a better understanding of the cellular and molecular mechanisms underlying tumor immunity has provided the appropriate framework for the development of therapeutic strategies for cancer immunotherapy. Under this complex scenario, galectins have emerged as promising molecular targets for cancer therapy responsible of creating immunosuppressive microenvironments at sites of tumor growth and metastasis. Galectins, expressed in tumor, stromal, and endothelial cells, contribute to thwart the development of immune responses by favoring the expansion of T regulatory cells and contributing to their immunosuppressive activity, driving the differentiation of tolerogenic dendritic cells, limiting T cell viability, and maintaining T cell anergy. The emerging data promise a future scenario in which the selective blockade of individual members of the galectin family, either alone or in combination with other therapeutic regimens, will contribute to halt tumor progression by counteracting tumor-immune escape. Here we describe a selection of methods used to investigate the role of galectin-1 in tumor-immune escape.