CONICET | Buscador de Institutos y Recursos Humanos

Endogenous Galectin-1 in T Lymphocytes Regulates Anti-prostate Cancer ImmunityThe design and evaluation of new immunotherapies for prostate cancer require a better understanding of the multiple molecular interactions between tumor cells and their associated microenvironment. In this context, prostate carcinoma produces Galectin-1 as one of the key molecules to escape the immune attack; therefore, it is essential to understand all the molecular processes in which this protein is involved. Most of the previous studies found in the literature have focused on the remodeling properties of the immune microenvironment by Galectin-1 secreted by the tumor, through its interactions with glyco-receptors at the cell membrane and the extracellular matrix. In this conference, I propose to discuss recent results of our research group that demonstrate a novel role of endogenous Galectin-1 in T lymphocytes in the control of anti-prostate cancer immunity. Indeed, using a preclinical murine model of prostate cancer, our results show that Galectin-1 of lymphocytes plays a fundamental role in the regulation of their proliferation rates and cytotoxic function. This functional regulation of lymphocyte Galectin-1 occurs under conditions of high concentration of extracellular Galectin-1, which is derived mainly from tumor cells. Under such conditions, the absence of Galectin-1 in T lymphocytes enhances anti-tumor immune responses. Our results demonstrate that endogenous Galectin-1 in CD4 + T lymphocytes, but mainly in CD8 + T cells, acts as a negative regulator of anti-tumor immunity. In conclusion, prostate tumors require T lymphocytes to express Galectin-1 to evade immune responses. These results lay the foundation for an original immunotherapy strategy for prostate cancer.