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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.
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Submitted May 29, 2007
Accepted July 30, 2007
Friend retrovirus infection of myeloid dendritic cells impairs maturation, prolongs contact to naive T cells, and favors expansion of regulatory T cells
Sandra Balkow, Frank Krux, Karin Loser, Jan Ulrich Becker, Stephan Grabbe, and Ulf Dittmer*
Department of Dermatology, University of Muenster, Muenster, Germany
Institute for Virology, University Duisburg- Essen, Essen, Germany
Institute of Pathology and Neuropathology, University Duisburg-Essen, Essen, Germany
Department of Dermatology, University of Mainz, Mainz, Germany
* Corresponding author; email: ulf.dittmer{at}uni-due.de.
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 (DC) 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 DC in virus-induced immunosuppression. About 20% of the myeloid DC that were generated from the bone marrow of FV-infected mice carried FV proteins. The infection was productive, and infected DC transmitted the virus in cell culture and in vivo. FV infection of DC led to a defect in DC maturation as infected cells expressed very little co-stimulatory molecules. Live imaging analysis of the cell contact between DC and T cells revealed prolonged contacts of T cells with infected DC as compared to uninfected DC. Although naive T cells were still activated by FV-infected DC this activation did not result in antigen-specific T cell proliferation. Interestingly, infected DC expanded a population of Foxp3-positive regulatory T cells with immunosuppressive potential suggesting that the contact between naive T cells and retrovirus-infected DC results in tolerance rather than immunity. Thus, retroviral infection of DC leads to an expansion of regulatory T cells, which might serve as an immune escape mechanism of the virus.
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