Evidence map›Paper›PMID 24794230›Full record

ArticleJournal of neuroimmunology2014

Apolipoprotein E mediation of neuro-inflammation in a murine model of multiple sclerosis.

Soomin Shin, Katharine A Walz, Angela S Archambault, Julia Sim, Bryan P Bollman, Jessica Koenigsknecht-Talboo, Anne H Cross, David M Holtzman, Gregory F Wu

Abstract read
In one paragraph

Article in Journal of neuroimmunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 18% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Science translational medicine · 2020
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Soomin ShinDepartment of Neurology, Washington University in St. Louis School of Medicine, Box 8111, 660 S. Euclid Avenue, St. Louis, MO 63110, United States.
Katharine A WalzDepartment of Neurology, Washington University in St. Louis School of Medicine, Box 8111, 660 S. Euclid Avenue, St. Louis, MO 63110, United States.
Angela S ArchambaultDepartment of Neurology, Washington University in St. Louis School of Medicine, Box 8111, 660 S. Euclid Avenue, St. Louis, MO 63110, United States.
Julia SimDepartment of Developmental Biology, Washington University in St. Louis School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, United States.
Bryan P BollmanDepartment of Neurology, Washington University in St. Louis School of Medicine, Box 8111, 660 S. Euclid Avenue, St. Louis, MO 63110, United States.
Jessica Koenigsknecht-TalbooDepartment of Neurology, Washington University in St. Louis School of Medicine, Box 8111, 660 S. Euclid Avenue, St. Louis, MO 63110, United States.
Anne H CrossDepartment of Neurology, Washington University in St. Louis School of Medicine, Box 8111, 660 S. Euclid Avenue, St. Louis, MO 63110, United States; Hope Center for Neurological Disorders, Washington University in St. Louis School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, United States.
David M HoltzmanDepartment of Neurology, Washington University in St. Louis School of Medicine, Box 8111, 660 S. Euclid Avenue, St. Louis, MO 63110, United States; Department of Developmental Biology, Washington University in St. Louis School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, United States; Hope Center for Neurological Disorders, Washington University in St. Louis School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, United States.
Gregory F WuDepartment of Neurology, Washington University in St. Louis School of Medicine, Box 8111, 660 S. Euclid Avenue, St. Louis, MO 63110, United States; Hope Center for Neurological Disorders, Washington University in St. Louis School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, United States; Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, United States. Electronic address: wug@neuro.wustl.edu.
Washington University in St. Louis · USHope Center for Neurological Disorders · US

Funding

Viral Discovery in Rheumatoid ArthritisP30AR048335 · NIAMS · WASHINGTON UNIVERSITY · PI BYUN, MINJI · 2001 to 2015
$8.9M
Effect of apoE on CNS neurons: Role of LRPR37AG013956 · NIA · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M. · 2004 to 2013
$3.8M
ROLE OF B CELL ANTIGEN PRESENTATION IN AUTOIMMUNE ENCEPHALOMYELITISR01NS083678 · NINDS · WASHINGTON UNIVERSITY · PI WU, GREGORY · 2013 to 2017
$1.7M
APOE EFFECT ON CNS NEURONS--ROLE OF LRPR01AG013956 · NIA · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M · 1996 to 2003
$1.2M
T cell regulation by dendritic cells in EAEK08NS062138 · NINDS · WASHINGTON UNIVERSITY · PI WU, GREGORY · 2008 to 2012
$831k
NIAMS NIH HHS P30 AR048335NIAMS NIH HHS P30AR048335NIA NIH HHS AG13956NIA NIH HHS R01 AG013956NIA NIH HHS R37 AG013956NINDS NIH HHS 5K08NS062138NINDS NIH HHS K08 NS062138NINDS NIH HHS R01 NS083678
6 · The paper itself

Abstract

Apolipoprotein E (ApoE) functions as a ligand in receptor-mediated endocytosis of lipoprotein particles and has been demonstrated to play a role in antigen presentation. To explore the contribution of ApoE during autoimmune central nervous system (CNS) demyelination, we examined the clinical, cellular immune function, and pathologic consequences of experimental autoimmune encephalomyelitis (EAE) induction in ApoE knockout (ApoE(-/-)) mice. We observed reduced clinical severity of EAE in ApoE(-/-) mice in comparison to WT mice that was concomitant with an early reduction of dendritic cells (DCs) followed by a reduction of additional innate cells in the spinal cord at the peak of disease without any differences in axonal damage. While T cell priming was enhanced in ApoE(-/-) mice, reduced severity of EAE was also observed in ApoE(-/-) recipients of encephalitogenic wild type T cells. Expression of ApoE during EAE was elevated within the CNS of wild type mice, particularly by innate cells such as DCs. Overall, ApoE promotes clinical EAE, likely by mediation of inflammation localized within the CNS.

Indexed as

AnimalsAntigen PresentationApolipoproteins ECD4-Positive T-LymphocytesCentral Nervous SystemCX3C Chemokine Receptor 1Dendritic CellsDisease Models, AnimalDose-Response Relationship, ImmunologicEncephalitisEncephalomyelitis, Autoimmune, ExperimentalFreund's AdjuvantLeukocytes, MononuclearMiceMice, Inbred C57BLMice, TransgenicApolipoproteins ECX3C Chemokine Receptor 1Cx3cr1 protein, mouseFreund's AdjuvantReceptors, ChemokineAntigen presentationApolipoprotein EDendritic cellsEAE

Identifiers

PMID24794230
PMCPMC4042395
OpenAlexW2008256259

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.