DEFINING THE FATE AND FUNCTION OF EFFECTOR T CELLS THROUGH GALECTIN-1 ? GALECTIN-1 LIGAND BINDING INTERACTIONS: IMPLICATIONS IN TUMOR IMMUNITY

DIMITROFF, C; RABINOVICH, GA

Tumor-Induced Immune Suppression. Mechanisms and Therapeutic Reversal?

Springer

Lugar: Tampa; Año: 2013;

Interactions between galectin-1 (Gal-1) and Gal-1 ligands on T cells are critically involved in regulating the intensity of T cell-mediated inflammation and anti-tumor immunity. Select T cell membrane proteins displayed on N- and/or O-linked glycans, operationally defined as Gal-1 ligands, bind Gal-1 and elicit downstream cellular activities that dampen effector T cell function. Together, these biological constituents represent promising targets in the development of novel anti-inflammatory and anti-tumor immune therapies. Whether through characteristic elevations in tumor-derived Gal-1 or an imbalance in regulatory and Gal-1 ligand+ effector T cell subsets during inflammation, the Gal-1 ? Gal-1 ligand binding axis offers numerous cellular/tissue contexts to strategically interfere with Gal-1 efficacy. In this review, we will examine recent assessments of: (1) Gal-1 expression and function in controlling both adaptive and anti-tumor T cell immunity, (2) Identity and function of T cell Gal-1 ligands, and (3) Targeting of the Gal-1 ? Gal-1 ligand axis to regulate inflammation or boost anti-tumor immune responses. These research disciplines collectively highlight the importance of understanding the identity and functional nature of Gal-1 and its ligands to strategically and safely manipulate the immune system to control immunopathologic conditions.