Evidence map›Paper›PMID 10885659›Full record

ArticleBrain pathology (Zurich, Switzerland)2000

Antibody association with a novel model for primary progressive multiple sclerosis: induction of relapsing-remitting and progressive forms of EAE in H2s mouse strains.

I Tsunoda, L Q Kuang, D J Theil, R S Fujinami

Open access · greenAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Experimental Autoimmune Encephalomyelitis in Mice.Methods in molecular biology (Clifton, N.J.) · 2016
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Immunity and inflammation in neurodegenerative diseases.American journal of neurodegenerative disease · 2013
    Article
  19. Article
  20. Review
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

4 authors at 1 institution in 1 country.

I TsunodaDepartment of Neurology, University of Utah School of Medicine, Salt Lake City 84132, USA.
L Q Kuang
D J Theil
R S Fujinami
University of Utah · US

Funding

NIAID NIH HHS AI42525
6 · The paper itself

Abstract

Multiple sclerosis (MS) can be divided into 4 clinical forms: relapsing-remitting (RR), primary progressive (PP), secondary progressive (SP), and progressive relapsing (PR). Since PP-MS is notably different from the other forms of MS, both clinically and pathologically, the question arises whether PP-MS is immunologically similar to the other forms. The pathogenesis of the PP-MS remains unclear, partly due to a lack of highly relevant animal models. Using an encephalitogenic peptide from myelin oligodendrocyte glycoprotein (MOG)92-106, we have established animal models that mimic different forms of MS in 2 strains of H-2s mice, SJL/J and A.SW. We induced experimental allergic encephalomyelitis (EAE) using MOG92-106 in the presence or absence of supplemental Bordetella pertussis (BP). Although, SJL/J mice developed RR-EAE whether BP was given or not, A.SW mice developed PP-EAE without BP and SP-EAE with BP. Histologically, SJL/J mice developed mild demyelinating disease with T cell infiltration, while A.SW mice developed large areas of plaque-like demyelination with immunoglobulin deposition and neutrophil infiltration, but with minimal T cell infiltration. In A.SW mice without BP, high titer serum anti-MOG antibody was detected and the anti-MOG IgG2a/IgG1 ratio correlated with survival times of mice. We hypothesized that, in A.SW mice, a Th2 response favors production of myelinotoxic antibodies, leading to progressive forms with early death. Our new models indicate that a single encephalitogen could induce either RR-, PP-, or SP- forms of demyelinating disease in hosts with immunologically different humoral immune responses.

Indexed as

AnimalsAntibodiesCentral Nervous SystemDisease Models, AnimalDNA, BacterialEncephalomyelitis, Autoimmune, ExperimentalFemaleImmunoglobulinsIn Situ Nick-End LabelingLymphocytesMiceMice, Mutant StrainsMultiple Sclerosis, Chronic ProgressiveMultiple Sclerosis, Relapsing-RemittingMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinAntibodiesDNA, BacterialImmunoglobulinsMog protein, mouseMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsPeptide Fragments

Identifiers

PMID10885659
PMCPMC8098387
OpenAlexW2028061046

What OpenQuestion holds

Textmetadata
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.