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Blood, 1 June 2005, Vol. 105, No. 11, pp. 4399-4406. Prepublished online as a Blood First Edition Paper on February 3, 2005; DOI 10.1182/blood-2004-10-3854. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-10-3854v1 105/11/4399    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 Esplugues, E. Articles by Lauzurica, P. Search for Related Content PubMed PubMed Citation Articles by Esplugues, E. Articles by Lauzurica, P. Related Collections Immunobiology Immunotherapy Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Induction of tumor NK-cell immunity by anti-CD69 antibody therapy Enric Esplugues, Javier Vega-Ramos, David Cartoixà, Berta N. Vazquez, Ignasi Salaet, Pablo Engel, and Pilar Lauzurica From the Departamento de Fisiología, Universidad de Barcelona, Spain; and Immunology Unit, Department of Cellular Biology and Pathology, Medical School, Institut d'Investigacions Biomediques August Pi i Sunyer, Barcelona, Spain. The leukocyte activation marker CD69 is a novel regulator of the immune response, modulating the production of cytokines including transforming growth factor- (TGF-). We have generated an antimurine CD69 monoclonal antibody (mAb), CD69.2.2, which down-regulates CD69 expression in vivo but does not deplete CD69-expressing cells. Therapeutic administration of CD69.2.2 to wild-type mice induces significant natural killer (NK) cell–dependent antitumor responses to major histocompatibility complex (MHC) class I low RMA-S lymphomas and to RM-1 prostatic carcinoma lung metastases. These in vivo antitumor responses are comparable to those seen in CD69-/- mice. Enhanced host NK cytotoxic activity correlates with a reduction in NK-cell TGF- production and is independent of tumor priming. In vitro studies demonstrate the novel ability of anti-CD69 mAbs to activate resting NK cells in an Fc receptor–independent manner, resulting in a substantial increase in both NK-cell cytolytic activity and interferon (IFN) production. Modulation of the innate immune system with monoclonal antibodies to host CD69 thus provides a novel means to antagonize tumor growth and metastasis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. North, I. Bakhsh, C. Marden, H. Pittman, E. Addison, C. Navarrete, R. Anderson, and M. W. Lowdell Tumor-Primed Human Natural Killer Cells Lyse NK-Resistant Tumor Targets: Evidence of a Two-Stage Process in Resting NK Cell Activation J. Immunol., January 1, 2007; 178(1): 85 - 94. [Abstract] [Full Text] [PDF] H. F. Rosenberg Interview with Dr. Francisco Sanchez-Madrid regarding Pivotal Advance: CD69 targeting differentially affects the course of collagen-induced arthritis J. Leukoc. Biol., December 1, 2006; 80(6): 1231 - 1232. [Full Text] [PDF] D. Sancho, M. Gomez, G. Martinez del Hoyo, A. Lamana, E. Esplugues, P. Lauzurica, C. Martinez-A, and F. Sanchez-Madrid CD69 targeting differentially affects the course of collagen-induced arthritis J. Leukoc. Biol., December 1, 2006; 80(6): 1233 - 1241. [Abstract] [Full Text] [PDF]

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