ArticleProceedings of the National Academy of Sciences of the United States of America2002
Lymph nodal prion replication and neuroinvasion in mice devoid of follicular dendritic cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 142 citations in OpenAlex.
- Limited transmission of cervid prions to nonhuman primates provides insights into the zoonotic potential of chronic wasting disease.Science advances · 2026Article
- Prion diseases: Lessons from historical outbreaks and potential emerging ones.Protein science : a publication of the Protein Society · 2025Review
- Prion diseases disrupt glutamate/glutamine metabolism in skeletal muscle.PLoS pathogens · 2024Article
- Single-domain antibodies and aptamers drive new opportunities for neurodegenerative disease research.Frontiers in immunology · 2024Review
- Article
- The role of cellular prion protein in immune system.BMB reports · 2023Review
- Brain aging is faithfully modelled in organotypic brain slices and accelerated by prions.Communications biology · 2022Article
- THαβ Immunological Pathway as Protective Immune Response against Prion Diseases: An Insight for Prion Infection Therapy.Viruses · 2022Review
- Neuroinflammation in Prion Disease.International journal of molecular sciences · 2021Review
- Neuroimmune Response Mediated by Cytokines in Natural Scrapie after Chronic Dexamethasone Treatment.Biomolecules · 2021Article
- MicroRNA-155: Regulation of Immune Cells in Sepsis.Mediators of inflammation · 2021Review
- The Effects of Immune System Modulation on Prion Disease Susceptibility and Pathogenesis.International journal of molecular sciences · 2020Review
- Prion strain-dependent tropism is maintained between spleen and granuloma and relies on lymphofollicular structures.Scientific reports · 2019Article
- IVIG Delays Onset in a Mouse Model of Gerstmann-Sträussler-Scheinker Disease.Molecular neurobiology · 2019Article
- Review
- Oxidative and Inflammatory Events in Prion Diseases: Can They Be Therapeutic Targets?Current aging science · 2019Review
- How do PrPPathogens (Basel, Switzerland) · 2017Review
- The immunobiology of prion diseases.Nature reviews. Immunology · 2013Review
- Immunization with recombinant prion protein leads to partial protection in a murine model of TSEs through a novel mechanism.PloS one · 2013Article
- Rapamycin delays disease onset and prevents PrP plaque deposition in a mouse model of Gerstmann-Sträussler-Scheinker disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Variant Creutzfeldt-Jakob disease and scrapie are typically initiated by extracerebral exposure to prions, and exhibit early prion accumulation in germinal centers. Follicular dendritic cells (FDCs), whose development and maintenance in germinal centers depends on tumor necrosis factor (TNF) and lymphotoxin (LT) signaling, are thought to be indispensable for extraneural prion pathogenesis. Here, we administered prions intraperitoneally to mice deficient for TNF and LT signaling components. LT alpha(-/-), LT beta(-/-), LT betaR(-/-), and LT alpha(-/-) x TNFalpha(-/-) mice resisted infection and contained no infectivity in spleens and lymph nodes (when present). However, TNFR1(-/-), TNFR2(-/-), and some TNFalpha(-/-) mice developed scrapie similarly to wild-type mice. High prion titers were detected in lymph nodes, but not spleens, of TNFR1(-/-) and TNF alpha(-/-) mice despite absence of FDCs and germinal centers. Transfer of TNFR1(-/-) fetal liver cells into lethally irradiated Prnp(0/0) mice restored infectivity mainly in lymph nodes. Prion protein (PrP) colocalized with a minority of macrophages in tumor necrosis factor receptor (TNFR) 1(-/-) lymph nodes. Therefore, prion pathogenesis can be restricted to lymphoreticular subcompartments, and mature follicular dendritic cells are dispensable for this process. Macrophage subsets are plausible candidates for lymphoreticular prion pathogenesis and neuroinvasion in the absence of FDCs, and may represent a novel target for postexposure prophylaxis.
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