ArticlePLoS pathogens2011
Follicular dendritic cell-specific prion protein (PrP) expression alone is sufficient to sustain prion infection in the spleen.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 102 citations in OpenAlex.
- The axonal transport velocity of prions is independent of prion formation.PLoS pathogens · 2026Article
- CpG oligodeoxynucleotide reduces PrPMolecules and cells · 2026Article
- Delayed progression of prion disease in mice by polyarginine-facilitated prevention of PrPNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Acute LPS exposure enhances susceptibility to peripheral prion infection.Scientific reports · 2025Article
- Cases of Creutzfeldt-Jakob disease in young individuals: open questions regarding aetiology.Frontiers in cellular neuroscience · 2025Article
- Perspectives on CRISPR Genome Editing to Prevent Prion Diseases in High-Risk Individuals.Biomedicines · 2024Article
- Review
- The role of cellular prion protein in immune system.BMB reports · 2023Review
- The murine meninges acquire lymphoid tissue properties and harbour autoreactive B cells during chronic Trypanosoma brucei infection.PLoS biology · 2023Article
- Microglia deficiency accelerates prion disease but does not enhance prion accumulation in the brain.Glia · 2022Article
- The multiple functions of PrPJournal of molecular medicine (Berlin, Germany) · 2022Review
- Foot-and-mouth disease virus localisation on follicular dendritic cells and sustained induction of neutralising antibodies is dependent on binding to complement receptors (CR2/CR1).PLoS pathogens · 2022Article
- Transport of Prions in the Peripheral Nervous System: Pathways, Cell Types, and Mechanisms.Viruses · 2022Review
- THαβ Immunological Pathway as Protective Immune Response against Prion Diseases: An Insight for Prion Infection Therapy.Viruses · 2022Review
- Prion Infectivity and PrPInternational journal of molecular sciences · 2021Article
- Potential for transmission of sporadic Creutzfeldt-Jakob disease through peripheral routes.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- Neuroprotective effect and potential of cellular prion protein and its cleavage products for treatment of neurodegenerative disorders part I. a literature review.Expert review of neurotherapeutics · 2021Review
- Differentiation and activation of fibroblastic reticular cells.Immunological reviews · 2021Review
- The degree of astrocyte activation is predictive of the incubation time to prion disease.Acta neuropathologica communications · 2021Article
- The Effects of Immune System Modulation on Prion Disease Susceptibility and Pathogenesis.International journal of molecular sciences · 2020Review
4 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Prion diseases are characterised by the accumulation of PrP(Sc), an abnormally folded isoform of the cellular prion protein (PrP(C)), in affected tissues. Following peripheral exposure high levels of prion-specific PrP(Sc) accumulate first upon follicular dendritic cells (FDC) in lymphoid tissues before spreading to the CNS. Expression of PrP(C) is mandatory for cells to sustain prion infection and FDC appear to express high levels. However, whether FDC actively replicate prions or simply acquire them from other infected cells is uncertain. In the attempts to-date to establish the role of FDC in prion pathogenesis it was not possible to dissociate the Prnp expression of FDC from that of the nervous system and all other non-haematopoietic lineages. This is important as FDC may simply acquire prions after synthesis by other infected cells. To establish the role of FDC in prion pathogenesis transgenic mice were created in which PrP(C) expression was specifically "switched on" or "off" only on FDC. We show that PrP(C)-expression only on FDC is sufficient to sustain prion replication in the spleen. Furthermore, prion replication is blocked in the spleen when PrP(C)-expression is specifically ablated only on FDC. These data definitively demonstrate that FDC are the essential sites of prion replication in lymphoid tissues. The demonstration that Prnp-ablation only on FDC blocked splenic prion accumulation without apparent consequences for FDC status represents a novel opportunity to prevent neuroinvasion by modulation of PrP(C) expression on FDC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.