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Journal of Virology, May 2007, p. 4877-4880, Vol. 81, No. 9
0022-538X/07/$08.00+0 doi:10.1128/JVI.02345-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Kristen M. Kerksiek,2
Thomas Brocker,2 and
Hans Kretzschmar1*
Center for Neuropathology and Prion Research,1 Institute of Immunology, Ludwig Maximilians University, München, Germany2
Received 26 October 2006/ Accepted 6 February 2007
Controversial results have been observed in mouse models regarding the role of lymphoid tissues in prion pathogenesis. To investigate the role of dendritic cells (DC), we used a transgenic mouse model. In this model (CD11c-N17Rac1), a significant reduction of CD8+ CD11chi DC has been described, and the remaining CD8+ DC demonstrate a reduced capacity for the uptake of apoptotic cells. After intraperitoneal prion infection, significantly longer incubation times were observed in CD11c-N17Rac1 mice than in controls, indicating that a defect in CD8+ CD11chi DC significantly impedes neuroinvasion after intraperitoneal infection. In contrast, no distinct differences were observed between CD11c-N17Rac1 mice and controls after oral infection. This provides evidence that oral and intraperitoneal prion infections differ in lymphoreticular requirements.
Published ahead of print on 14 February 2007.
Current address: Institute of Medical Microbiology and Hygiene, University of Saarland, Homburg/Saar, Germany.
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