Fig. 1

Focusing on Galectin-3—mediated mechanisms of tumor immune escape occurring in TME. Panel A) Soluble Galectin-3 interacts with specific glycoligands on TCR. The derived lattice impairs an efficient TCR activation. Apoptosis of T-cells can be triggered when Galectin-3 interacts with specific O-linked sugar residues carried by CD45 receptor. Galectin-3 binding to specific glycoligands expressed on regulatory T-cells promotes expansion of this cell population favoring tumor immune escape. Panel B Galectin-3 interacts with the checkpoint molecule LAG3 expressed on antigen committed CD8 + T cells suppressing their function. Panel C Galectin-3 released in the TME by macrophages, stromal cells and tumor cells binds to β-galactosyl residues on extracellular matrix components, IFN-γ and glycosylated chemokines. The derived lattice forms a suppressive TME creating a gradient that impairs an efficient exposure of tumor cells to cytotoxic T-cells. Panel D) Galectin-3 plays as soluble ligand of NKp30 and NKG2D, two important NK-activating receptors. Galectin-3 reduces the affinity of the major histocompatibility complex class 1-related chain A (MICA) for NKG2D, silencing NK cells