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Blood, 15 November 2005, Vol. 106, No. 10, pp. 3465-3473. Prepublished online as a Blood First Edition Paper on July 21, 2005; DOI 10.1182/blood-2005-03-0855. This Article Full Text (PDF) Supplemental Tables All Versions of this Article: 2005-03-0855v1 106/10/3465    most recent Alert me when this article is cited Alert me if a correction is posted 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 Hanna, J. Articles by Mandelboim, O. Search for Related Content PubMed PubMed Citation Articles by Hanna, J. Articles by Mandelboim, O. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted March 1, 2005 Accepted July 8, 2005 Functional aberrant expression of CCR2 receptor on chronically activated NK cells in TAP2-deficient patients Jacob Hanna, Huda Mussaffi, Guy Steuer, Suhair Hanna, Maher Deeb, Hannah Blau, Tal I Arnon, Noam Weizman, and Ofer Mandelboim* The Lautenberg Center for General and Tumor Immunology, The Hebrew University - Hadassah Medical School, Jerusalem, Israel Pulmonary Unit, Schneider Children's Medical Center of Israel, Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel Department of Pediatrics, Assaf Harofe Hospital, Zrifin, Israel Department of Pediatrics, Rambam Medical Center, B. Rappaport School of Medicine, Haifa, Israel Department of Cardiothoracic Surgery, Shaare Zedek Medical Center, Jerusalem, Israel * Corresponding author; email: oferman{at}md2.huji.ac.il. Chemokines play a pivotal role in homeostatic and inflammatory migration of naive and activated NK subsets. Recent studies have shown that aberrant chemokine receptor expression on certain immune cells underlies the pathogenesis of clinical conditions in which recruitment of such cells is altered. A progressive accumulation of activated NK cells, subsequently resulting in the formation of chronic granoulomatous lesions in the respiratory tract and the skin, has been described in a number of TAP2-deficient patients at later stages of their disease. Therefore, the present study was set out to elucidate whether dysregulation of chemo-attracting receptors expression on NK cells could explain abnormal navigation of these cells in TAP2-deficiency. High-throughput proteomic comparison, followed by verification with flow-cytometry, revealed that chronically activated NK cells derived from three newly identified TAP2-deficient patients consistently expressed aberrant levels of CCR2 chemokine receptor in vitro and in vivo. This expression pattern translated into specific responsiveness of chronically activated NK cells derived from TAP2-deficient patients to multiple ligands of CCR2. Moreover, the in vivo elevated levels of IL-2 and MCP-1 detected in serum and bronchio-alveolar lavage samples derived from these patients highlight the potential involvement of CCR2 pathway in aberrant NK cell retention at chronic inflammatory sites. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Iannello, O. Debbeche, S. Samarani, and A. Ahmad Antiviral NK cell responses in HIV infection: I. NK cell receptor genes as determinants of HIV resistance and progression to AIDS J. Leukoc. Biol., July 1, 2008; 84(1): 1 - 26. [Abstract] [Full Text] [PDF]

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