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Alteration of B-Cell Subsets Enhances Neuroinvasion in Mouse Scrapie Infection

Christine von Poser-Klein,¹ Eckhard Flechsig,¹ Tanja Hoffmann,¹ Petra Schwarz,² Harry Harms,¹ Raymond Bujdoso,³ Adriano Aguzzi,^2, and Michael A. Klein^1,*

Institute of Virology and Immunobiology, University of Würzburg, D-97078 Würzburg, Germany,¹ Institute of Neuropathology, Department of Pathology, University Hospital of Zürich, Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland,² Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 OES, United Kingdom³

Received 14 September 2007/ Accepted 24 December 2007

Acquired forms of prion diseases or transmissible spongiform encephalopathies are believed to occur following peripheral exposure. Prions initially accumulate in the lymphoid system before spreading to the nervous system, but the underlying mechanisms for prion transfer between the two systems are still elusive. Here we show that ablation of the B-cell-specific transmembrane protein CD19, a coreceptor of the complement system, results in an acceleration of prion neuroinvasion. This appears to be due to an alteration of the follicular dendritic cell (FDC) network within the lymphoid tissue, thereby reducing the distance between FDCs and adjacent nerve fibers that mediate prion neuroinvasion.

Published ahead of print on 16 January 2008.

These two senior authors contributed equally to this study.