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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Smyth, M. J. Articles by Godfrey, D. I. Search for Related Content PubMed PubMed Citation Articles by Smyth, M. J. Articles by Godfrey, D. I. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 February 2002, Vol. 99, No. 4, pp. 1259-1266 IMMUNOBIOLOGY Sequential production of interferon- by NK1.1+ T cells and natural killer cells is essential for the antimetastatic effect of -galactosylceramide Mark J. Smyth, Nadine Y. Crowe, Daniel G. Pellicci, Konstantinos Kyparissoudis, Janice M. Kelly, Kazuyoshi Takeda, Hideo Yagita, and Dale I. Godfrey From Cancer Immunology, Trescowthick Laboratories, Peter MacCallum Cancer Institute, East Melbourne, Victoria, Australia; the Department of Pathology and Immunology, Monash Medical School, Prahran, Victoria, Australia; and the Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan. The antimetastatic effect of the CD1d-binding glycolipid, -galactosylceramide (-GalCer), is mediated by NK1.1+T (NKT) cells; however, the mechanisms behind this process are poorly defined. Although it has been shown to involve NK cells and interferon- (IFN-) production, the way these factors collaborate to mediate effective tumor rejection and the importance of other factors characteristic of NKT cell and NK cell activation are unknown. Using gene-targeted mice and antibody treatments, the critical need for interleukin 12 (IL-12), IFN-, and NK cells has been shown in the antimetastatic activity of -GalCer in the lungs and the liver. By contrast, in lung and liver metastasis models, cytotoxic molecules expressed by NK cells and NKT cells (perforin, Fas ligand, and tumor necrosis factor-related apoptosis-inducing ligand) and an NKT cell-secreted cytokine, IL-4, were not necessary for the antitumor activity of -GalCer. Like IL-12, IL-18 was required for optimal serum IFN- induction and control of lung metastases by -GalCer. IL-18 was unnecessary for -GalCer-related suppression of liver metastases. Most importantly, after adoptive transfer of -GalCer-reactive NKT cells or NK cells into NKT cell-deficient, IFN--deficient, or RAG-1-deficient mice, it was demonstrated that the sequential production of IFN- by NKT cells and NK cells was absolutely required to reconstitute the antimetastatic activity of -GalCer. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. Cullen, E. Germanov, T. Shimaoka, and B. Johnston Enhanced Tumor Metastasis in Response to Blockade of the Chemokine Receptor CXCR6 Is Overcome by NKT Cell Activation J. Immunol., November 1, 2009; 183(9): 5807 - 5815. [Abstract] [Full Text] [PDF] H. Yuling, X. Ruijing, L. Li, J. Xiang, Z. Rui, W. Yujuan, Z. Lijun, D. Chunxian, T. Xinti, X. Wei, et al. EBV-Induced Human CD8+ NKT Cells Suppress Tumorigenesis by EBV-Associated Malignancies Cancer Res., October 15, 2009; 69(20): 7935 - 7944. 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