ArticleThe American journal of pathology2003
Oral prion infection requires normal numbers of Peyer's patches but not of enteric lymphocytes.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 135 citations in OpenAlex.
- Prion protein fragment (106-126) activates NLRP3 inflammasome and promotes platelet-monocyte/neutrophil interactions, potentially contributing to an inflammatory state.Frontiers in cell and developmental biology · 2025Article
- New views on the complex interplay between degeneration and autoimmunity in multiple sclerosis.Frontiers in cellular neuroscience · 2024Article
- Issues for patchy tissues: defining roles for gut-associated lymphoid tissue in neurodevelopment and disease.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- THαβ Immunological Pathway as Protective Immune Response against Prion Diseases: An Insight for Prion Infection Therapy.Viruses · 2022Review
- The Effects of Immune System Modulation on Prion Disease Susceptibility and Pathogenesis.International journal of molecular sciences · 2020Review
- Primary structural differences at residue 226 of deer and elk PrP dictate selection of distinct CWD prion strains in gene-targeted mice.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Effect of co-infection with a small intestine-restricted helminth pathogen on oral prion disease pathogenesis in mice.Scientific reports · 2019Article
- Generation of novel neuroinvasive prions following intravenous challenge.Brain pathology (Zurich, Switzerland) · 2018Article
- Oral Prion Neuroinvasion Occurs Independently of PrPJournal of virology · 2018Article
- How do PrPPathogens (Basel, Switzerland) · 2017Review
- Prion disease pathogenesis in the absence of the commensal microbiota.The Journal of general virology · 2017Article
- Oral Prion Disease Pathogenesis Is Impeded in the Specific Absence of CXCR5-Expressing Dendritic Cells.Journal of virology · 2017Article
- Pathways of Prion Spread during Early Chronic Wasting Disease in Deer.Journal of virology · 2017Article
- Prion disease: experimental models and reality.Acta neuropathologica · 2017Review
- PrPC expression and prion seeding activity in the alimentary tract and lymphoid tissue of deer.PloS one · 2017Article
- Increased Abundance of M Cells in the Gut Epithelium Dramatically Enhances Oral Prion Disease Susceptibility.PLoS pathogens · 2016Article
- Prions efficiently cross the intestinal barrier after oral administration: Study of the bioavailability, and cellular and tissue distribution in vivo.Scientific reports · 2016Article
- Article
- The Gut-Associated Lymphoid Tissues in the Small Intestine, Not the Large Intestine, Play a Major Role in Oral Prion Disease Pathogenesis.Journal of virology · 2015Article
- The immunobiology of prion diseases.Nature reviews. Immunology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prion pathogenesis following oral exposure is thought to involve gut-associated lymphatic tissue, which includes Peyer's patches (PPs) and M cells. Recruitment of activated B lymphocytes to PPs requires alpha(4)beta(7) integrin; PPs of beta 7(-/-) mice are normal in number but are atrophic and almost entirely devoid of B cells. Here we report that minimal infectious dose and disease incubation after oral exposure to logarithmic dilutions of prion inoculum were similar in beta 7(-/-) and wild-type mice, and PPs of both beta 7(-/-) and wild-type mice contained 3-4 log LD(50)/g prion infectivity > or =125 days after challenge. Despite marked reduction of B cells, M cells were present in beta 7(-/-) mice. In contrast, mice deficient in both tumor necrosis factor and lymphotoxin-alpha (TNF alpha(-/-) x LT alpha(-/-)) or in lymphocytes (RAG-1(-/-), mu MT), in which numbers of PPs are reduced in number, were highly resistant to oral challenge, and their intestines were virtually devoid of prion infectivity at all times after challenge. Therefore, lymphoreticular requirements for enteric and for intraperitoneal uptake of prions differ from each other. Although susceptibility to prion infection following oral challenge correlates with the number of PPs, it is remarkably independent of the number of PP-associated lymphocytes.
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