SEARCH:   Advanced

Blood, 15 April 2007, Vol. 109, No. 8, pp. 3333-3341. Prepublished online as a Blood First Edition Paper on December 12, 2006; DOI 10.1182/blood-2006-06-026385. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2006-06-026385v1 109/8/3333    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 Xu, J. Articles by Vujanovic, N. L. Search for Related Content PubMed PubMed Citation Articles by Xu, J. Articles by Vujanovic, N. L. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Essential role of the TNF-TNFR2 cognate interaction in mouse dendritic cell–natural killer cell crosstalk Jun Xu1,3, Ayan K. Chakrabarti1, Jennifer L. Tan1, Lisheng Ge1,2, Andrea Gambotto4,5, and Nikola L. Vujanovic1,2 1 University of Pittsburgh Cancer Institute and 2 Department of Pathology, University of Pittsburgh School of Medicine, PA; 3 First Affiliate Hospital, Guangzhou Medical College, China; 4 Department of Surgery and 5 Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, PA Dendritic cells (DCs) and natural killer (NK) cells are essential components of the innate immune system and have a central role in initiation and regulation of adaptive immune responses. During the early critical immune activities, DCs and NK cells interact and reciprocally regulate each other via cell-cell contact. The molecular mediators of the DC–NK-cell crosstalk are largely undefined. In the present study, we show in mice that DC stimulation of NK-cell IFN- secretion requires DC membranebound but not secreted products; is increased by augmenting the expression of DC transmembrane tumor necrosis factor (tmTNF) and NK-cell transmembrane TNF receptor type 2 (tmTNFR2); is inhibited by blocking TNF or TNFR2 but not TNFR1; is impaired by knocking out DC Tnf or NK-cell Tnfr2 but not DC Tnfr1 or Tnfr2 and NK-cell Tnf or Tnfr1; and is restored in TNF-deficient DCs by reconstituting tmTNF, but cannot be mimicked by soluble TNF. We also demonstrate that DC TNF and NK-cell TNFR2 are required for DC-mediated NK-cell proliferation and amplification of cytotoxic activity. These novel findings provide the first evidence that DC–NK-cell crosstalk mediates enhancement of NK-cell functions via triggering NK-cell tmTNFR2 by DC tmTNF. 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: II. viral strategies for evasion and lessons for immunotherapy and vaccination J. Leukoc. Biol., July 1, 2008; 84(1): 27 - 49. [Abstract] [Full Text] [PDF] A. Shanker, G. Verdeil, M. Buferne, E.-M. Inderberg-Suso, D. Puthier, F. Joly, C. Nguyen, L. Leserman, N. Auphan-Anezin, and A.-M. Schmitt-Verhulst CD8 T Cell Help for Innate Antitumor Immunity J. Immunol., November 15, 2007; 179(10): 6651 - 6662. [Abstract] [Full Text] [PDF]

	Copyright © 2007 by American Society of Hematology         Online ISSN: 1528-0020