@article{oai:toyama.repo.nii.ac.jp:00015752,
 author = {Ogura, Keisuke and Sato-Matsushita, Marimo and Yamamoto, Seiji and Hori, Takashi and Sasahara, Masakiyo and Iwakura, Yoichiro and Saiki, Ikuo and Tahara, Hideaki and Hayakawa, Yoshihiro},
 issue = {3},
 journal = {Cancer Immunology Research},
 month = {Mar},
 note = {application/pdf, Although NK cells are recognized as direct antitumor effectors, the ability of NK cells to control cancer-associated inflammation, which facilitates tumor progression, remains unknown. In this study, we demonstrate that NK cells control tumor-promoting inflammation through functional modification of neutrophils. NK cells control the tumor-promoting function of neutrophils through an IFNgamma-dependent mechanism. Tumor progression in an NK cell-depleted host is diminished when the IL17A-neutrophil axis is absent. In NK cell-depleted mice, neutrophils acquire a tumor-promoting phenotype, characterized by up-regulation of VEGF-A expression, which promotes tumor growth and angiogenesis. A VEGFR inhibitor which preferentially suppressed tumor growth in NK cell-depleted mice was dependent on neutrophils. Furthermore, the systemic neutropenia caused by an anti-metabolite treatment showed an anti-cancer effect only in mice lacking NK cells. Thus, NK cells likely control the tumor-promoting and angiogenic function of neutrophils., Article, Cancer Immunology Research , DOI: 10.1158/2326-6066.CIR-17-0204},
 title = {NK cells control tumor-promoting function of neutrophils in mice},
 volume = {6},
 year = {2018}
}