ArticleJournal of virology2000
Follicular dendritic cells and dissemination of Creutzfeldt-Jakob disease.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 65 citations in OpenAlex.
- Delayed progression of prion disease in mice by polyarginine-facilitated prevention of PrPNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Review
- Proliferative arrest of neural cells induces prion protein synthesis, nanotube formation, and cell-to-cell contacts.Journal of cellular biochemistry · 2010Article
- The kuru infectious agent is a unique geographic isolate distinct from Creutzfeldt-Jakob disease and scrapie agents.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Role of the lymphoreticular system in prion neuroinvasion from the oral and nasal mucosa.Journal of virology · 2009Article
- Strain-specific viral properties of variant Creutzfeldt-Jakob disease (vCJD) are encoded by the agent and not by host prion protein.Journal of cellular biochemistry · 2009Article
- Form follows function: lymphoid tissue microarchitecture in antimicrobial immune defence.Nature reviews. Immunology · 2008Review
- Prion infection of oral and nasal mucosa.Journal of virology · 2006Article
- Prion diseases: current understanding of epidemiology and pathogenesis, and therapeutic advances.CNS drugs · 2006Review
- Two Creutzfeldt-Jakob disease agents reproduce prion protein-independent identities in cell cultures.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Early induction of interferon-responsive mRNAs in Creutzfeldt-Jakob disease.Journal of neurovirology · 2004Article
- Follicular dendritic cell dedifferentiation by treatment with an inhibitor of the lymphotoxin pathway dramatically reduces scrapie susceptibility.Journal of virology · 2003Article
- Virus-like interference in the latency and prevention of Creutzfeldt-Jakob disease.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Unique inflammatory RNA profiles of microglia in Creutzfeldt-Jakob disease.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Rapid prion neuroinvasion following tongue infection.Journal of virology · 2003Article
- Microglia from Creutzfeldt-Jakob disease-infected brains are infectious and show specific mRNA activation profiles.Journal of virology · 2002Article
- Retrograde transport of transmissible mink encephalopathy within descending motor tracts.Journal of virology · 2002Article
- Lymphotoxin-alpha- and lymphotoxin-beta-deficient mice differ in susceptibility to scrapie: evidence against dendritic cell involvement in neuroinvasion.Journal of virology · 2002Article
- Lymph nodal prion replication and neuroinvasion in mice devoid of follicular dendritic cells.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Infected splenic dendritic cells are sufficient for prion transmission to the CNS in mouse scrapie.The Journal of clinical investigation · 2001Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The contribution of immune system cells to the propagation of transmissible encephalopathies is not well understood. To determine how follicular dendritic cells (FDC) may act, we challenged lymphotoxin beta null and wild-type (wt) controls with a Creutzfeldt-Jakob disease (CJD) agent. There was only a small difference in incubation time to clinical disease even after peripheral challenge with low infectious doses (31 in a total of 410 days). Brain pathology with extensive microglial infiltration, identified by keratan sulfate, as well as astrocytic hypertrophy, was also equivalent in all groups despite the fact that null mice had neither FDC nor splenic metallophilic macrophages that filter particulate antigen. Because FDC accumulate pathologic prion protein (PrP) in infected but not wt mice, we studied the cellular distribution of PrP by confocal microscopy. The majority of pathologic PrP collected on the plasma membrane of FDC, as identified by the Ca(+2)-binding protein S100A. This surface distribution suggested that agent aggregated with pathologic PrP might spread by cell-to-cell contacts. While several types of leukocytes may be involved in agent dissemination, cells of myeloid lineage were found to be infectious. Moreover, perivascular tracks of microglia and abnormal PrP after intraperitoneal inoculation were consistent with hematogenous spread. In summary, FDC are not required for CJD agent spread from the periphery, although FDC may enhance spread through surface accumulation of pathologic PrP. While it is still not clear where the infectious agent replicates, macrophages can sequester appreciable levels of infectivity and hence act as reservoirs for prolonged latent infection.
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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.