| First Author | Eckelhart E | Year | 2011 |
| Journal | Blood | Volume | 117 |
| Issue | 5 | Pages | 1565-73 |
| PubMed ID | 21127177 | Mgi Jnum | J:169574 |
| Mgi Id | MGI:4941295 | Doi | 10.1182/blood-2010-06-291633 |
| Citation | Eckelhart E, et al. (2011) A novel Ncr1-Cre mouse reveals the essential role of STAT5 for NK-cell survival and development. Blood 117(5):1565-73 |
| abstractText | We generated a transgenic mouse line that expresses the Cre recombinase under the control of the Ncr1 (p46) promoter. Cre-mediated recombination was tightly restricted to natural killer (NK) cells, as revealed by crossing Ncr1-iCreTg mice to the eGFP-LSLTg reporter strain. Ncr1-iCreTg mice were further used to study NK cell-specific functions of Stat5 (signal transducers and activators of transcription 5) by generating Stat5(f/f) Ncr1-iCreTg animals. Stat5(f/f) Ncr1-iCreTg mice were largely devoid of NK cells in peripheral lymphoid organs. In the bone marrow, NK-cell maturation was abrogated at the NK cell-precursor stage. Moreover, we found that in vitro deletion of Stat5 in interleukin 2-expanded NK cells was incompatible with NK-cell viability. In vivo assays confirmed the complete abrogation of NK cell-mediated tumor control against B16F10-melanoma cells. In contrast, T cell-mediated tumor surveillance against MC38-adenocarcinoma cells was undisturbed. In summary, the results of our study show that STAT5 has a cell-intrinsic role in NK-cell development and that Ncr1-iCreTg mice are a powerful novel tool with which to study NK-cell development, biology, and function. |
