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Blood, 1 December 2007, Vol. 110, No. 12, pp. 3949-3958. Prepublished online as a Blood First Edition Paper on August 15, 2007; DOI 10.1182/blood-2007-05-092189. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2007-05-092189v1 110/12/3949    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 Balkow, S. Articles by Dittmer, U. Search for Related Content PubMed PubMed Citation Articles by Balkow, S. Articles by Dittmer, U. Related Collections Immunobiology Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Friend retrovirus infection of myeloid dendritic cells impairs maturation, prolongs contact to naïve T cells, and favors expansion of regulatory T cells Sandra Balkow1, Frank Krux2, Karin Loser1, Jan U. Becker3, Stephan Grabbe4, and Ulf Dittmer2 1 Department of Dermatology, University of Muenster, Muenster; 2 Institute for Virology and 3 Institute of Pathology and Neuropathology, University Duisburg-Essen, Essen; and 4 Department of Dermatology, University of Mainz, Mainz, Germany Retroviruses have developed immunmodulatory mechanisms to avoid being attacked by the immune system. The mechanisms of this retrovirus-associated immune suppression are far from clarified. Dendritic cells (DCs) have been attributed a decisive role in these pathogenic processes. We have used the Friend retrovirus (FV) mouse model in order to acquire further knowledge about the role of infection of DCs in virus-induced immunosuppression. About 20% of the myeloid DCs that were generated from the bone marrow of FV-infected mice carried FV proteins. The infection was productive, and infected DCs transmitted the virus in cell culture and in vivo. FV infection of DCs led to a defect in DC maturation, as infected cells expressed very little costimulatory molecules. Live imaging analysis of the cell contact between DCs and T cells revealed prolonged contacts of T cells with infected DCs compared with uninfected DCs. Although naive T cells were still activated by FV-infected DCs, this activation did not result in antigen-specific T-cell proliferation. Interestingly, infected DCs expanded a population of Foxp3+ regulatory T cells with immunosuppressive potential, suggesting that the contact between naive T cells and retrovirus-infected DCs results in tolerance rather than immunity. Thus, retroviral infection of DCs leads to an expansion of regulatory T cells, which might serve as an immune escape mechanism of the virus. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Retroviral escape by Friendly infected DCs Simon C. Barry and P. Toby H. Coates Blood 2007 110: 3819-3820. [Full Text] [PDF] This article has been cited by other articles: G. Cabrera, D. Burzyn, J. Mundinano, M. C. Courreges, G. Camicia, D. Lorenzo, H. Costa, S. R. Ross, I. Nepomnaschy, and I. Piazzon Early Increases in Superantigen-Specific Foxp3+ Regulatory T Cells during Mouse Mammary Tumor Virus Infection J. Virol., August 1, 2008; 82(15): 7422 - 7431. [Abstract] [Full Text] [PDF] S. Li, E. J. Gowans, C. Chougnet, M. Plebanski, and U. Dittmer Natural Regulatory T Cells and Persistent Viral Infection J. Virol., January 1, 2008; 82(1): 21 - 30. [Full Text] [PDF]

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