ArticleThe American journal of pathology2008
Absence of the cellular prion protein exacerbates and prolongs neuroinflammation in experimental autoimmune encephalomyelitis.
Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 59 citations in OpenAlex.
- Prion protein modulation of virus-specific T cell differentiation and function during acute viral infection.ImmunoHorizons · 2025Article
- Prion protein alters viral control and enhances pathology after perinatal cytomegalovirus infection.Nature communications · 2024Article
- New Light on Prions: Putative Role of PrPInternational journal of molecular sciences · 2024Review
- Comprehensive Analysis of Soluble Mediator Profiles in Congenital CMV Infection Using an MCMV Model.Viruses · 2024Article
- The role of cellular prion protein in immune system.BMB reports · 2023Review
- An LRP1-binding motif in cellular prion protein replicates cell-signaling activities of the full-length protein.JCI insight · 2023Article
- HTLV-1 p12 modulates the levels of prion protein (PrPFrontiers in microbiology · 2023Article
- The multiple functions of PrPJournal of molecular medicine (Berlin, Germany) · 2022Review
- Newly Identified Deficiencies in the Multiple Sclerosis Central Nervous System and Their Impact on the Remyelination Failure.Biomedicines · 2022Review
- A Soluble PrPJournal of immunology (Baltimore, Md. : 1950) · 2022Article
- New Epidermal-Growth-Factor-Related Insights Into the Pathogenesis of Multiple Sclerosis: Is It Also Epistemology?Frontiers in neurology · 2021Review
- Microglia in Prion Diseases: Angels or Demons?International journal of molecular sciences · 2020Review
- Vitamin D3 receptor polymorphisms regulate T cells and T cell-dependent inflammatory diseases.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Binding between Prion Protein and Aβ Oligomers Contributes to the Pathogenesis of Alzheimer's Disease.Virologica Sinica · 2019Review
- Mechanisms of neuroprotection against ischemic insult by stress-inducible phosphoprotein-1/prion protein complex.Journal of neurochemistry · 2018Article
- Stress Resilience of Spermatozoa and Blood Mononuclear Cells without Prion Protein.Frontiers in molecular biosciences · 2018Article
- Physiological Functions of the Cellular Prion Protein.Frontiers in molecular biosciences · 2017Review
- Regulation of Amyloid β Oligomer Binding to Neurons and Neurotoxicity by the Prion Protein-mGluR5 Complex.The Journal of biological chemistry · 2016Article
- The Cellular Prion Protein: A Player in Immunological Quiescence.Frontiers in immunology · 2015Review
- Cellular prion protein (PrP(C)) and its role in stress responses.International journal of clinical and experimental medicine · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the physiological roles of the cellular prion protein (PrP C) remain to be fully elucidated, PrP C has been proposed to represent a potential regulator of cellular immunity. To test this hypothesis, we evaluated the consequences of PrP C deficiency on the course of experimental autoimmune encephalomyelitis induced by immunization with myelin oligodendrocyte glycoprotein peptide. Consistent with augmented proliferative responses and increased cytokine gene expression by myelin oligodendrocyte glycoprotein-primed Prnp-/- T cells, PrP C-deficient mice demonstrated more aggressive disease onset and a lack of clinical improvement during the chronic phase of experimental autoimmune encephalomyelitis. Acutely, Prnp-/- spinal cord, cerebellum, and forebrain exhibited higher levels of leukocytic infiltrates and pro-inflammatory cytokine gene expression, as well as increased spinal cord myelin basic protein and axonal loss. During the chronic phase, a remarkable persistence of leukocytic infiltrates was present in the forebrain and cerebellum, accompanied by an increase in interferon-gamma and interleukin-17 transcripts. Attenuation of T cell-dependent neuroinflammation thus represents a potential novel function of PrP C.
Indexed as
Identifiers
What OpenQuestion holds
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.