ArticleJournal of virology2002
Lymphotoxin-alpha- and lymphotoxin-beta-deficient mice differ in susceptibility to scrapie: evidence against dendritic cell involvement in neuroinvasion.
Article in Journal of virology, 2002. 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
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
22 citing papers in PubMed, 52 citations in OpenAlex.
- The Effects of Immune System Modulation on Prion Disease Susceptibility and Pathogenesis.International journal of molecular sciences · 2020Review
- Review
- Prion disease and the innate immune system.Viruses · 2012Review
- Lymphotoxin, but not TNF, is required for prion invasion of lymph nodes.PLoS pathogens · 2012Article
- Characteristics of 263K scrapie agent in multiple hamster species.Emerging infectious diseases · 2009Article
- Splenic CD19-CD35+B220+ cells function as an inducer of follicular dendritic cell network formation.Blood · 2007Article
- Levels of abnormal prion protein in deer and elk with chronic wasting disease.Emerging infectious diseases · 2007Article
- Role of the CD8+ dendritic cell subset in transmission of prions.Journal of virology · 2007Article
- Early and rapid engraftment of bone marrow-derived microglia in scrapie.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Processing of the bovine spongiform encephalopathy-specific prion protein by dendritic cells.Journal of virology · 2006Article
- Role of lymphotoxin in experimental models of infectious diseases: potential benefits and risks of a therapeutic inhibition of the lymphotoxin-beta receptor pathway.Infection and immunity · 2005Review
- Molecular neurology of prion disease.Journal of neurology, neurosurgery, and psychiatry · 2005Review
- Neuroinvasion by scrapie following inoculation via the skin is independent of migratory Langerhans cells.Journal of virology · 2005Article
- Measles virus interacts with human SLAM receptor on dendritic cells to cause immunosuppression.Virology · 2004Article
- Follicular dendritic cell dedifferentiation by treatment with an inhibitor of the lymphotoxin pathway dramatically reduces scrapie susceptibility.Journal of virology · 2003Article
- T cells infiltrate the brain in murine and human transmissible spongiform encephalopathies.Journal of virology · 2003Article
- Rapid prion neuroinvasion following tongue infection.Journal of virology · 2003Article
- Transmission of prions.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Comparison of abnormal prion protein glycoform patterns from transmissible spongiform encephalopathy agent-infected deer, elk, sheep, and cattle.Journal of virology · 2002Article
- Processing and degradation of exogenous prion protein by CD11c(+) myeloid dendritic cells in vitro.Journal of virology · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Transmissible spongiform encephalopathy or prion diseases are fatal neurodegenerative disorders of humans and animals often initiated by oral intake of an infectious agent. Current evidence suggests that infection occurs initially in the lymphoid tissues and subsequently in the central nervous system (CNS). The identity of infected lymphoid cells remains controversial, but recent studies point to the involvement of both follicular dendritic cells (FDC) and CD11c(+) lymphoid dendritic cells. FDC generation and maintenance in germinal centers is dependent on lymphotoxin alpha (LT-alpha) and LT-beta signaling components. We report here that by the oral route, LT-alpha -/- mice developed scrapie while LT-beta -/- mice did not. Furthermore, LT-alpha -/- mice had a higher incidence and shorter incubation period for developing disease following inoculation than did LT-beta -/- mice. Transplantation of lymphoid tissues from LT-beta -/- mice, which have cervical and mesenteric lymph nodes, into LT-alpha -/- mice, which do not, did not alter the incidence of CNS scrapie. In other studies, a virus that is tropic for and alters functions of CD11c(+) cells did not alter the kinetics of neuroinvasion of scrapie. Our results suggest that neither FDC nor CD11c(+) cells are essential for neuroinvasion after high doses of RML scrapie. Further, it is possible that an as yet unidentified cell found more abundantly in LT-alpha -/- than in LT-beta -/- mice may assist in the amplification of scrapie infection in the periphery and favor susceptibility to CNS disease following peripheral routes of infection.
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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.