ArticleHistochemistry and cell biology2010
Spreading of prions from the immune to the peripheral nervous system: a potential implication of dendritic cells.
Article in Histochemistry and cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Proof-of-Concept Human Organ-on-Chip Study: First Step of Platform to Assess Neuro-Immunological Communication Involved in Inflammatory Bowel Diseases.International journal of molecular sciences · 2023Article
- Intracellular and Intercellular Mitochondrial Dynamics in Parkinson's Disease.Frontiers in neuroscience · 2019Review
- Expression of genes involved in the T cell signalling pathway in circulating immune cells of cattle 24 months following oral challenge with Bovine Amyloidotic Spongiform Encephalopathy (BASE).BMC veterinary research · 2015Article
- Immunotherapy in prion disease.Nature reviews. Neurology · 2013Review
- Misfolded protein aggregates: mechanisms, structures and potential for disease transmission.Seminars in cell & developmental biology · 2011Review
- Histochemistry and cell biology: the annual review 2010.Histochemistry and cell biology · 2011Review
- Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The implication of dendritic cells (DCs) in the peripheral spreading of prions has increased in the last few years. It has been recently described that DCs can transmit prions to primary neurons from the central nervous system. In order to improve the understanding of the earliest steps of prion peripheral neuroinvasion, we studied, using an in vitro model, the effect of exposing primary peripheral neurons to scrapie-infected lymphoid cells. Thanks to this system, there is evidence that bone marrow dendritic cells (BMDCs) are in connection with neurites of peripheral neurons via cytoplasmic extensions. BMDCs are competent to internalize prions independently from the expression of cellular prion protein (PrP(C)) and have the capacity to transmit detergent-insoluble, relatively proteinase K-resistant prion protein (PrP(Sc)) to peripheral neurons after 96 h of coculture. Furthermore, we confirmed the special status of the peripheral nervous system in front of prion diseases. Contrary to central neurons, PrP(Sc) infection does not disturb survival and neurite outgrowth. Our model demonstrates that PrP(Sc)-loaded dendritic cells and peripheral nerve fibers that are included in neuroimmune interfaces can initiate and spread prion neuroinvasion.
Indexed as
Identifiers
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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.