| First Author | Prinz D | Year | 2020 |
| Journal | Eur J Immunol | Volume | 50 |
| Issue | 6 | Pages | 880-890 |
| PubMed ID | 32052406 | Mgi Jnum | J:299430 |
| Mgi Id | MGI:6490863 | Doi | 10.1002/eji.201948222 |
| Citation | Prinz D, et al. (2020) Loss of NKG2D in murine NK cells leads to increased perforin production upon long-term stimulation with IL-2. Eur J Immunol 50(6):880-890 |
| abstractText | NK cells are innate lymphocytes responsible for lysis of pathogen-infected and transformed cells. One of the major activating receptors required for target cell recognition is the NK group 2D (NKG2D) receptor. Numerous reports show the necessity of NKG2D for effective tumor immune surveillance. Further studies identified NKG2D as a key element allowing tumor immune escape. We here use a mouse model with restricted deletion of NKG2D in mature NKp46(+) cells (NKG2D(DeltaNK) ). NKG2D(DeltaNK) NK cells develop normally, have an unaltered IFN-gamma production but kill tumor cell lines expressing NKG2D ligands (NKG2DLs) less efficiently. However, upon long-term stimulation with IL-2, NKG2D-deficient NK cells show increased levels of the lytic molecule perforin. Thus, our findings demonstrate a dual function of NKG2D for NK cell cytotoxicity; while NKG2D is a crucial trigger for cytotoxicity of tumor cells expressing activating ligands it is also capable to limit perforin production in IL-2 activated NK cells. |
