| First Author | Takeda K | Year | 2011 |
| Journal | J Leukoc Biol | Volume | 90 |
| Issue | 4 | Pages | 777-85 |
| PubMed ID | 21712396 | Mgi Jnum | J:177544 |
| Mgi Id | MGI:5295361 | Doi | 10.1189/jlb.0411208 |
| Citation | Takeda K, et al. (2011) IFN-gamma production by lung NK cells is critical for the natural resistance to pulmonary metastasis of B16 melanoma in mice. J Leukoc Biol 90(4):777-85 |
| abstractText | NK cells are effector lymphocytes playing a critical role in the natural resistance against tumors. However, the precise mechanisms underlying NK cell-mediated natural resistance against tumor metastasis are still unrevealed. B16 cells, mouse melanoma cells, were resistant to freshly isolated NK cell-mediated killing; nevertheless, NK cells were critical for natural resistance against experimental lung metastasis of B16 cells. We found that lung metastasis was increased significantly in IFN-gamma(-/-) mice but not pfp(-/-), IFN-alphaR(-/-), or IL-12/IL-18(-/-) mice. Interestingly, freshly isolated lung NK cells, but not spleen or liver NK cells, displayed augmented IFN-gamma production after B16 inoculation. Adoptive transfer of pfp(-/-) NK cells, but not IFN-gamma(-/-) NK cells, significantly decreased B16 lung metastasis in IFN-gamma(-/-) and pfp/IFN-gamma(-/-)mice. Lung metastases of IFN-gammaRDN B16 was also increased in NK cell-depleted or IFN-gamma(-/-) mice, suggesting that the IFN-gamma response of host cells was required in the NK cell and IFN-gamma-mediated antimetastatic effect. Our results demonstrate that IFN-gamma production from lung resident NK cells is a key response in the natural resistance to the experimental lung metastasis of NK cell-resistant tumor cells. |
