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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 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 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 Hanna, J. Articles by Mandelboim, O. Search for Related Content PubMed PubMed Citation Articles by Hanna, J. Articles by Mandelboim, O. Related Collections Immunobiology Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Functional aberrant expression of CCR2 receptor on chronically activated NK cells in patients with TAP-2 deficiency Jacob Hanna, Huda Mussaffi, Guy Steuer, Suhair Hanna, Maher Deeb, Hannah Blau, Tal I. Arnon, Noam Weizman, and Ofer Mandelboim From the Lautenberg Center for General and Tumor Immunology, Hebrew University–Hadassah Medical School, Jerusalem, Israel; the Pulmonary Unit, Schneider Children's Medical Center of Israel, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel; the Department of Pediatrics, Assaf Harofe Hospital, Zrifin, Israel; the Department of Pediatrics, Rambam Medical Center, B. Rappaport School of Medicine, Technion, Haifa, Israel; and the Department of Cardiothoracic Surgery, Shaare Zedek Medical Center, Jerusalem, Israel. Chemokines play a pivotal role in homeostatic and inflammatory migration of naive and activated natural killer (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. Progressive accumulation of activated NK cells, subsequently resulting in the formation of chronic granulomatous lesions in the respiratory tract and the skin, has been described in a number of patients with transporter associated with antigen processing 2 (TAP-2) deficiency in the later stages of disease. Therefore, the goal of the present study was to elucidate whether the dysregulation of chemoattracting receptor expression on NK cells could explain abnormal navigation of these cells in TAP-2 deficiency. High-throughput proteomic comparison, followed by verification with flow cytometry, revealed that chronically activated NK cells derived from 3 newly identified patients with TAP-2 deficiency consistently expressed aberrant levels of CC chemokine receptor 2 (CCR2) chemokine receptor in vitro and in vivo. This expression pattern translated into specific responsiveness of chronically activated NK cells derived from patients with TAP-2 deficiency to multiple ligands of CCR2. Moreover, the in vivo elevated levels of interleukin-2 (IL-2) and monocyte chemoattractant protein-1 (MCP-1) detected in serum and bronchoalveolar lavage samples derived from these patients highlight the potential involvement of the 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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