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Blood, 15 April 2005, Vol. 105, No. 8, pp. 3011-3018. Prepublished online as a Blood First Edition Paper on December 16, 2004; DOI 10.1182/blood-2004-10-4072. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-10-4072v1 105/8/3011    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 Trotta, R. Articles by Caligiuri, M. A. Search for Related Content PubMed PubMed Citation Articles by Trotta, R. Articles by Caligiuri, M. A. Related Collections Signal Transduction Free Research Articles Plenary Papers Immunobiology Phagocytes Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  PLENARY PAPERS Differential expression of SHIP1 in CD56bright and CD56dim NK cells provides a molecular basis for distinct functional responses to monokine costimulation Rossana Trotta, Robin Parihar, Jianhua Yu, Brian Becknell, Jeffrey Allard, II, Jing Wen, Wei Ding, Hsiaoyin Mao, Susheela Tridandapani, William E. Carson, and Michael A. Caligiuri From the Division of Human Cancer Genetics, Department of Molecular Virology, Immunology, and Medical Genetics; Medical Scientific Program, Integrated Biomedical Graduate Program, College of Medicine and Public Health; Division of Pulmonary and Critical Care, Department of Internal Medicine; The Comprehensive Cancer Center, The Ohio State University; Division of Surgical Oncology, Department of Surgery; and Division of Hematology/Oncology, Department of Internal Medicine, The Ohio State University, Columbus, OH. Monocyte cytokines (ie, monokines) induce natural killer (NK) cells to produce interferon- (IFN-), which is critical for monocyte clearance of infectious pathogens and tumor surveillance. Human CD56bright NK cells produce far more IFN- in response to monokines than do CD56dim NK cells. The kinases and phosphatases involved in regulating IFN- production by monokine-activated NK cells are not clearly identified. SHIP1 is a 5' inositol phosphatase that dephosphorylates the phosphatidylinositol-3 kinase (PI-3K) product PI3,4,5P3. Here, we show that constitutive expression of SHIP1 is distinctly lower in CD56bright NK cells compared with CD56dim NK cells, suggesting it could be an important negative regulator of IFN- production in monokine-activated NK cells. Indeed, overexpression of SHIP1 in CD56bright NK cells followed by monokine activation substantially lowered IFN- production. This effect was not seen when NK cells were infected with a SHIP1 mutant containing an inactive catalytic domain. Finally, NK cells in SHIP1–/– mice produced more IFN- in response to monokines in vivo than did NK cells from wild-type mice. Collectively, these results demonstrate that SHIP1 negatively regulates monokine-induced NK cell IFN- production in vitro and in vivo and provide the first molecular explanation for an important functional distinction observed between CD56bright and CD56dim human NK subsets. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: NK cell cytokine secretion regulated by SHIP1 Jerome Ritz Blood 2005 105: 3003. [Full Text] [PDF] This article has been cited by other articles: S. V. Kondadasula, J. M. Roda, R. Parihar, J. Yu, A. Lehman, M. A. Caligiuri, S. Tridandapani, R. W. Burry, and W. E. Carson III Colocalization of the IL-12 receptor and Fc{gamma}RIIIa to natural killer cell lipid rafts leads to activation of ERK and enhanced production of interferon-{gamma} Blood, April 15, 2008; 111(8): 4173 - 4183. [Abstract] [Full Text] [PDF] P. Schierloh, N. Yokobori, M. Aleman, V. Landoni, L. Geffner, R. M. Musella, J. Castagnino, M. Baldini, E. Abbate, S. S. de la Barrera, et al. 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