Chemotherapy-elicited upregulation of NKG2D and DNAM-1 ligands as a therapeutic target in multiple myeloma
A Soriani, C Fionda, B Ricci, ML Iannitto… - …, 2013 - Taylor & Francis
A Soriani, C Fionda, B Ricci, ML Iannitto, M Cippitelli, A Santoni
Oncoimmunology, 2013•Taylor & FrancisMalignant 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.
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.
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.
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