Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 108, Issue 5, Pages 703-708Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI200113155
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Funding
- NIAMS NIH HHS [R01 AR002594, AR02594] Funding Source: Medline
- NIA NIH HHS [R01 AG015408, AG15408] Funding Source: Medline
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Transmissible 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-1(0/0) 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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