Pierre Aucouturier, Frédéric Geissmann, Diane Damotte, Gabriela P. Saborio, Harry C. Meeker, Regina Kascsak, Richard Kascsak, Richard I. Carp, Thomas Wisniewski
J Clin Invest.
2001;
108(5):703–708
doi:10.1172/JCI13155
This article Copyright © 2001, The American Society for Clinical Investigation
Abstract
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T
ransmissible spongiform encephalopathies display long incubation periods at the beginning of which the titer of infectious agents (prions) increases in peripheral lymphoid organs. This “replication” leads to a progressive invasion of the CNS. Follicular dendritic cells appear to support prion replication in lymphoid follicles. However, the subsequent steps of neuroinvasion remain obscure. CD11c+ dendritic cells, an unrelated cell type, are candidate vectors for prion propagation. We found a high infectivity titer in splenic dendritic cells from prion-infected mice, suggesting that dendritic cells carry infection. To test this hypothesis, we injected RAG-10/0 mice intravenously with live spleen cell subsets from scrapie-infected donors. Injection of infected dendritic cells induced scrapie without accumulation of prions in the spleen. These results suggest that CD11c+ dendritic cells can propagate prions from the periphery to the CNS in the absence of any additional lymphoid element.
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