ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Genetic depletion of complement receptors CD21/35 prevents terminal prion disease in a mouse model of chronic wasting disease.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- Tissue-specific biochemical differences between chronic wasting disease prions isolated from free-ranging white-tailed deer (Odocoileus virginianus).The Journal of biological chemistry · 2022Article
- Neuroinflammation in Prion Disease.International journal of molecular sciences · 2021Review
- The Effects of Immune System Modulation on Prion Disease Susceptibility and Pathogenesis.International journal of molecular sciences · 2020Review
- PAD-Beads enrichment enhances detection of PrPBMC research notes · 2019Article
- Cellular and Molecular Mechanisms of Prion Disease.Annual review of pathology · 2019Review
- Let's make microglia great again in neurodegenerative disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Article
- Complement Regulatory Protein Factor H Is a Soluble Prion Receptor That Potentiates Peripheral Prion Pathogenesis.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- How do PrPPathogens (Basel, Switzerland) · 2017Review
- Oral Prion Disease Pathogenesis Is Impeded in the Specific Absence of CXCR5-Expressing Dendritic Cells.Journal of virology · 2017Article
- Increased Abundance of M Cells in the Gut Epithelium Dramatically Enhances Oral Prion Disease Susceptibility.PLoS pathogens · 2016Article
- Article
- Low activity of complement in the cerebrospinal fluid of the patients with various prion diseases.Infectious diseases of poverty · 2016Article
- Article
- Analysis of the Putative Role of CR1 in Alzheimer's Disease: Genetic Association, Expression and Function.PloS one · 2016Article
- Clay Components in Soil Dictate Environmental Stability and Bioavailability of Cervid Prions in Mice.Frontiers in microbiology · 2016Article
- Remarkable Activation of the Complement System and Aberrant Neuronal Localization of the Membrane Attack Complex in the Brain Tissues of Scrapie-Infected Rodents.Molecular neurobiology · 2015Article
- Prion amplification and hierarchical Bayesian modeling refine detection of prion infection.Scientific reports · 2015Article
- Murine complement receptor 1 is required for germinal center B cell maintenance but not initiation.Immunobiology · 2014Article
- The immunobiology of prion diseases.Nature reviews. Immunology · 2013Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
The complement system has been shown to facilitate peripheral prion pathogenesis. Mice lacking complement receptors CD21/35 partially resist terminal prion disease when infected i.p. with mouse-adapted scrapie prions. Chronic wasting disease (CWD) is an emerging prion disease of captive and free-ranging cervid populations that, similar to scrapie, has been shown to involve the immune system, which probably contributes to their relatively facile horizontal and environmental transmission. In this study, we show that mice overexpressing the cervid prion protein and susceptible to CWD (Tg(cerPrP)5037 mice) but lack CD21/35 expression completely resist clinical CWD upon peripheral infection. CD21/35-deficient Tg5037 mice exhibit greatly impaired splenic prion accumulation and replication throughout disease, similar to CD21/35-deficient murine prion protein mice infected with mouse scrapie. TgA5037;CD21/35(-/-) mice exhibited little or no neuropathology and deposition of misfolded, protease-resistant prion protein associated with CWD. CD21/35 translocate to lipid rafts and mediates a strong germinal center response to prion infection that we propose provides the optimal environment for prion accumulation and replication. We further propose a potential role for CD21/35 in selecting prion quasi-species present in prion strains that may exhibit differential zoonotic potential compared with the parental strains.
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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.