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Blood, 1 July 2006, Vol. 108, No. 1, pp. 246-252. Prepublished online as a Blood First Edition Paper on March 23, 2006; DOI 10.1182/blood-2005-11-4535. This Article Full Text Full Text (PDF) Supplemental Figure All Versions of this Article: 2005-11-4535v1 108/1/246    most recent 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 Richards, J. O. Articles by Liu, Y. Search for Related Content PubMed PubMed Citation Articles by Richards, J. O. Articles by Liu, Y. Related Collections Signal Transduction Immunobiology Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Tumor growth impedes natural-killer-cell maturation in the bone marrow John O. Richards, Xing Chang, Bradley W. Blaser, Michael A. Caligiuri, Pan Zheng, and Yang Liu From the Division of Cancer Immunology, Department of Pathology; and the Division of Hematology and Oncology, Department of Internal Medicine, The Ohio State University Medical Center and Comprehensive Cancer Center, Columbus. Natural-killer (NK)-cell dysfunction and IFN- deficiencies have been associated with increased incidence of both malignancy and infection. The immunologic basis of NK-cell defects in cancer-bearing hosts has not been extensively studied. Here, we demonstrate that multiple lineages of tumors, including thymoma, breast cancer, colon cancer, and melanoma cell lines, interrupt functional maturation during NK-cell development in the bone marrow. The immature NK cells in the periphery of tumor-bearing mice had impaired IFN- production but seemingly normal cytotoxicity. T cells are not involved in this NK maturation arrest, because T-cell depletion did not restore NK-cell development. Moreover, the extent of tumor-cell infiltration into the bone marrow does not correlate with defective NK maturation. Interestingly, the defect was associated with a significant reduction in the IL-15R+ cells in the non-T, non-NK compartment of bone marrow cells and restored by overexpression of IL-15. Our data demonstrate that tumor growth can impede functional maturation of NK cells, most likely by interrupting the requisite IL-15 signaling pathway. (Blood. 2006;108:246-252) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. M. El-Sherbiny, J. L. Meade, T. D. Holmes, D. McGonagle, S. L. Mackie, A. W. Morgan, G. Cook, S. Feyler, S. J. Richards, F. E. Davies, et al. The Requirement for DNAM-1, NKG2D, and NKp46 in the Natural Killer Cell-Mediated Killing of Myeloma Cells Cancer Res., September 15, 2007; 67(18): 8444 - 8449. [Abstract] [Full Text] [PDF] A Plonquet, C Haioun, J-P Jais, A-L Debard, G Salles, M-C Bene, P Feugier, C Rabian, O Casasnovas, M Labalette, et al. Peripheral blood natural killer cell count is associated with clinical outcome in patients with aaIPI 2 3 diffuse large B-cell lymphoma Ann. Onc., July 1, 2007; 18(7): 1209 - 1215. [Abstract] [Full Text] [PDF]

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