@article{ATM7765,
author = {Elke Pogge von Strandmann and Olga Shatnyeva and Hinrich Hansen},
title = {NKp30 and its ligands: emerging players in tumor immune evasion from natural killer cells},
journal = {Annals of Translational Medicine},
volume = {3},
number = {20},
year = {2015},
keywords = {},
abstract = {It is indisputable that natural killer (NK) immune surveillance is of crucial importance for hematological and solid tumors. However, the outcome of NK cell-based immune therapies appears disappointing in many trials. Limitations include poor in vivo survival or lack of specificity and are often attributed to tumor-associated immune escape mechanisms. NK cells are terminally activated by ligation of the activating NK receptors NKG2D, NKp30 or NKp46 through their corresponding ligands, which are up-regulated on the cell surface of dangerous cells (1-5). There is evidence that malignant cells bypass the NK surveillance by releasing these ligands as soluble proteins, as shown for NKG2D and NKp30 ligands (6-10). In most cases, the ligands are released by metalloproteinase-dependent shedding. The relevance of this mechanism was clearly confirmed in a transgenic animal model, showing spontaneous growth of tumors with the shedding-proficient NKG2D ligand MICA but tumor-free survival of animals with a shedding-resistant NKG2D ligand (11).},
issn = {2305-5847}, url = {https://atm.amegroups.org/article/view/7765}
}