Infected splenic dendritic cells are sufficient for prion transmission to the CNS in mouse scrapie

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 p...

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Bibliographic Details
Published in:The Journal of clinical investigation 2001-09, Vol.108 (5), p.703-708
Main Authors: Aucouturier, P, Geissmann, F, Damotte, D, Saborio, G P, Meeker, H C, Kascsak, R, Carp, R I, Wisniewski, T
Format: Article
Language:English
Subjects:
Adoptive Transfer
Animals
Dendritic Cells - chemistry
Dendritic Cells - physiology
Dendritic Cells - transplantation
Emerging diseases
Genes, RAG-1
Human health and pathology
Immunology
Infectious diseases
Integrin alphaXbeta2 - analysis
Life Sciences
Mice
Mice, Inbred C57BL
Mice, Knockout
Neurons and Cognition
Prions - pathogenicity
PrPSc Proteins - analysis
Scrapie - immunology
Scrapie - pathology
Scrapie - transmission
Spleen - anatomy & histology
Spleen - pathology
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Summary: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.
ISSN:0021-9738
DOI:10.1172/JCI200113155