Study of galectins in tumor immunity: strategies and methods

• Published in: Methods in molecular biology (Clifton, N.J.) Vol. 1207; p. 249
• Main Authors: Cerliani, Juan P, Dalotto-Moreno, Tomas, Compagno, Daniel, Dergan-Dylon, L Sebastián, Laderach, Diego J, Gentilini, Lucas, Croci, Diego O, Méndez-Huergo, Santiago P, Toscano, Marta A, Salatino, Mariana, Rabinovich, Gabriel A
• Format: Journal Article
• Language: English
• Published: United States 01-01-2015
• Subjects: Adoptive Transfer; Animals; Antigens, Neoplasm - immunology; Blotting, Western; Bone Marrow Cells - cytology; CD3 Complex - metabolism; Cell Proliferation; Cell Separation; Cytokines - metabolism; Dendritic Cells - cytology; Dendritic Cells - metabolism; Enzyme-Linked Immunosorbent Assay; Flow Cytometry; Galectin 1 - metabolism; Galectins - metabolism; Gene Silencing; Genetic Vectors - genetics; Humans; Interleukin-27 - metabolism; Lentivirus - genetics; Lymph Nodes - immunology; Mice; Neoplasms - immunology; Neoplasms - metabolism; Neoplasms - pathology; Phosphorylation; Spleen - immunology; STAT3 Transcription Factor - metabolism; T-Lymphocytes, Regulatory - cytology; T-Lymphocytes, Regulatory - immunology; T-Lymphocytes, Regulatory - metabolism; Transduction, Genetic; Tumor Microenvironment
• ISSN: 1940-6029
• DOI: 10.1007/978-1-4939-1396-1_16

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.