ArticleInternational immunology2013
Complement protein C3 exacerbates prion disease in a mouse model of chronic wasting disease.
Article in International immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 22 citations in OpenAlex.
- Time-dependent transcriptomic response to scrapie exposure in ovine MSC-derived neuron-like cells.Frontiers in cellular and infection microbiology · 2026Article
- 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
- Unaltered intravenous prion disease pathogenesis in the temporary absence of marginal zone B cells.Scientific reports · 2019Article
- Let's make microglia great again in neurodegenerative disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Molecular Alterations in the Cerebellum of Sporadic Creutzfeldt-Jakob Disease Subtypes with DJ-1 as a Key Regulator of Oxidative Stress.Molecular neurobiology · 2018Article
- 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
- Viral-derived complement inhibitors: current status and potential role in immunomodulation.Experimental biology and medicine (Maywood, N.J.) · 2017Review
- Article
- Reversible off and on switching of prion infectivity via removing and reinstalling prion sialylation.Scientific reports · 2016Article
- Low activity of complement in the cerebrospinal fluid of the patients with various prion diseases.Infectious diseases of poverty · 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
- Ablation of CCAAT/Enhancer-Binding Protein Delta (C/EBPD): Increased Plaque Burden in a Murine Alzheimer's Disease Model.PloS one · 2015Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Accumulating evidence shows a critical role of the complement system in facilitating attachment of prions to both B cells and follicular dendritic cells and assisting in prion replication. Complement activation intensifies disease in prion-infected animals, and elimination of complement components inhibits prion accumulation, replication and pathogenesis. Chronic wasting disease (CWD) is a highly infectious prion disease of captive and free-ranging cervid populations that utilizes the complement system for efficient peripheral prion replication and most likely efficient horizontal transmission. Here we show that complete genetic or transient pharmacological depletion of C3 prolongs incubation times and significantly delays splenic accumulation in a CWD transgenic mouse model. Using a semi-quantitative prion amplification scoring system we show that C3 impacts disease progression in the early stages of disease by slowing the rate of prion accumulation and/or replication. The delayed kinetics in prion replication correlate with delayed disease kinetics in mice deficient in C3. Taken together, these data support a critical role of C3 in peripheral CWD prion pathogenesis.
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.