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Blood, 1 June 2004, Vol. 103, No. 11, pp. 4207-4215. Prepublished online as a Blood First Edition Paper on February 12, 2004; DOI 10.1182/blood-2003-12-4350. This Article Full Text (PDF) Supplemental Figure All Versions of this Article: 2003-12-4350v1 103/11/4207    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 Senechal, B. Articles by Young, J. W Search for Related Content PubMed PubMed Citation Articles by Senechal, B. Articles by Young, J. W Social Bookmarking                   What's this? Submitted December 29, 2003 Accepted January 29, 2004 Infection of mature monocyte-derived dendritic cells with human cytomegalovirus inhibits stimulation of T-cell proliferation via the release of soluble CD83 Brigitte Senechal, Adam M Boruchov, John L Reagan, Derek N Hart, and James W Young* Laboratory of Cellular Immunobiology, Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY, USA Mater Medical Research Institute, South Brisbane, Queensland, Australia Laboratory of Cellular Immunobiology, Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY, USA; Allogeneic Transplantation and Clinical Immunology Services, Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY, USA; Weill Medical College of Cornell University, New York, NY, USA * Corresponding author; email: youngjw{at}mskcc.org. We have studied the mechanisms by which human cytomegalovirus (HCMV) infection of monocyte-derived dendritic cells (moDCs) contribute to immune suppression. Unlike infection of immature moDCs, infection of mature moDCs is not lytic and results in minimally decreased surface MHC and costimulatory molecule expression. The presence of a small percentage of CMV infected mature moDCs, or the transfer of supernatant from infected moDCs depleted of infectious virions, is nevertheless sufficient to cause marked inhibition of immunostimulation by normal, uninfected moDCs. Neither viral nor human IL-10, nor TGF-beta-1, could account for this inhibition. In contrast, we show that infected mature moDCs lose surface CD83, while maintaining intracellular protein expression. Soluble CD83 accumulates in the supernatants of CMV-infected mature moDCs, and CD83 immunodepletion removes the inhibitory effect of these supernatants on normal DC immunostimulation. We have thus discovered a new mechanism by which HCMV infection may establish a non-lytic reservoir in mature moDCs that inhibits DC-mediated T-cell responses. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Crough and R. Khanna Immunobiology of Human Cytomegalovirus: from Bench to Bedside Clin. Microbiol. Rev., January 1, 2009; 22(1): 76 - 98. [Abstract] [Full Text] [PDF] T. Kessler, M. Reich, G. Jahn, E. Tolosa, A. Beck, H. Kalbacher, H. Overkleeft, S. Schempp, and C. Driessen Human cytomegalovirus infection interferes with major histocompatibility complex type II maturation and endocytic proteases in dendritic cells at multiple levels J. Gen. Virol., October 1, 2008; 89(10): 2427 - 2436. [Abstract] [Full Text] [PDF] K. Luthje, B. Kretschmer, B. Fleischer, and M. Breloer CD83 regulates splenic B cell maturation and peripheral B cell homeostasis Int. Immunol., August 1, 2008; 20(8): 949 - 960. 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