In:
Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 90, No. 4 ( 2011-06-28), p. 777-785
Abstract:
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-γ–/– mice but not pfp–/–, IFN-αR–/–, or IL-12/IL-18–/– mice. Interestingly, freshly isolated lung NK cells, but not spleen or liver NK cells, displayed augmented IFN-γ production after B16 inoculation. Adoptive transfer of pfp–/– NK cells, but not IFN-γ–/– NK cells, significantly decreased B16 lung metastasis in IFN-γ–/– and pfp/IFN-γ–/–mice. Lung metastases of IFN-γRDN B16 was also increased in NK cell-depleted or IFN-γ–/– mice, suggesting that the IFN-γ response of host cells was required in the NK cell and IFN-γ-mediated antimetastatic effect. Our results demonstrate that IFN-γ 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.
Type of Medium:
Online Resource
ISSN:
0741-5400
,
1938-3673
Language:
English
Publisher:
Oxford University Press (OUP)
Publication Date:
2011
detail.hit.zdb_id:
2026833-6
SSG:
12
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