Chemotherapy-elicited upregulation of NKG2D and DNAM-1 ligands as a therapeutic target in multiple myeloma.

Malignant cells constitutively express Natural killer group 2, member D (NKG2D) or DNAX Accessory Molecule-1 (DNAM-1) ligands, yet they are often unable to trigger a robust cytotoxic cell response. It may be therapeutically useful to implement strategies aimed at increasing the density of NKG2D and DNAM-1 ligands on the surface of cancer cells, endowing them with the capacity to activate potent antitumor natural killer-cell responses.