Abstract
DC-SIGN (DC-specific intercellular adhesion molecule-3-grabbing nonintegrin), which is a type II transmembrane C-type lectin expressed on dendritic cells (DCs), recognizes cell-surface carbohydrates on invading pathogens such as bacteria and viruses and plays an important role in the uptake and presentation of these antigens. To date, little is known about the correlation of DC-SIGN with cancer. Recently, we reported that DC-SIGN bound to colorectal carcinoma cells by recognizing colorectal tumor-associated Lewis (Le) glycan ligands. The interaction of DC-SIGN with colorectal cancer cells increased LPS-induced IL-6 and IL-10 secretion from monocyte-derived DCs (MoDCs), resulting in inhibition of the maturation of MoDCs and differentiation of naïve T cells into Th1 cells. Furthermore, DC-SIGN-expressing cells were shown to colocalize with colorectal cancer-associated Le glycan ligands in primary colon cancer tissues. These results indicate that DC-SIGN-mediated dysfunction of DCs in tumor immunity is one of the critical mechanisms for escaping immune surveillance.
