ArticlePloS one2010
Prion replication in the hematopoietic compartment is not required for neuroinvasion in scrapie mouse model.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed.
- How do PrPPathogens (Basel, Switzerland) · 2017Review
- Oral Prion Disease Pathogenesis Is Impeded in the Specific Absence of CXCR5-Expressing Dendritic Cells.Journal of virology · 2017Article
- The Good, the Bad, and the Ugly of Dendritic Cells during Prion Disease.Journal of immunology research · 2015Review
- The immunobiology of prion diseases.Nature reviews. Immunology · 2013Review
- Ataxia with cerebellar lesions in mice expressing chimeric PrP-Dpl protein.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Prion disease and the innate immune system.Viruses · 2012Review
- Prion protein is a key determinant of alcohol sensitivity through the modulation of N-methyl-D-aspartate receptor (NMDAR) activity.PloS one · 2012Article
- Th2-polarised PrP-specific transgenic T-cells confer partial protection against murine scrapie.PLoS pathogens · 2011Article
- Sex effects in mouse prion disease incubation time.PloS one · 2011Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fatal neurodegenerative prion diseases are caused by the transmissible PrP(Sc) prion agent whose initial replication after peripheral inoculation takes place in follicular dendritic cells present in germinal centers of lymphoid organs. However, prion replication also occurs in lymphoid cells. To assess the role of the hematopoietic compartment in neuroinvasion and prion replication, we generated chimeric mice, on a uniform congenic C57/BL6J background, by bone marrow replacement with hematopoietic cells expressing different levels of PrP protein. Nine different types of chimeric mice were inoculated intraperitoneally either with the lymphotropic Rocky Mountain Laboratory (RML) strain or the non lymphotropic ME-7 scrapie strain, at different doses. Here, we clearly demonstrate that overexpression of PrP by the hematopoietic system, or the lack of PrP expression by the bone marrow derived cells, does not change the incubation time period of the disease, even when the mice are infected at limiting doses. We conclude that the hematopoietic compartment is more or less permissive to prion replication, both for RML and ME-7, but does not play a role in neuroinvasion.
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Registered trials
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.