Evidence map›Paper›PMID 11403222›Full record

ReviewJournal of clinical immunology2001

Immune responses against the myelin/oligodendrocyte glycoprotein in experimental autoimmune demyelination.

H C von Büdingen, N Tanuma, P Villoslada, J C Ouallet, S L Hauser, C P Genain

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of clinical immunology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Cranial nerve involvement in patients with MOG antibody-associated disease.Neurology(R) neuroimmunology & neuroinflammation · 2019
    Article
  5. Review
  6. Case Report: Acute Transverse Myelitis after Zika Virus Infection.The American journal of tropical medicine and hygiene · 2018
    Article
  7. Regulatory T-cell vaccination independent of auto-antigen.Experimental & molecular medicine · 2014
    Review
  8. MOBP-specific cellular immune responses are weaker than MOG-specific cellular immune responses in patients with multiple sclerosis and healthy subjects.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2013
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. B cells as a target of immune modulation.Annals of Indian Academy of Neurology · 2009
    Article
  17. Article
  18. Review
  19. Tolerance in the absence of autoantigen.Endocrine, metabolic & immune disorders drug targets · 2007
    Review
  20. Identification of a pathogenic antibody response to native myelin oligodendrocyte glycoprotein in multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2006
    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

6 authors at 1 institution in 1 country.

H C von BüdingenDepartment of Neurology, University of California, San Francisco 94143, USA.
N Tanuma
P Villoslada
J C Ouallet
S L Hauser
C P Genain
University of California, San Francisco · US

Funding

MECHANISMS OF EAER01AI043073 · NIAID · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI GENAIN, CLAUDE PAUL · 1997 to 2007
$2.4M
NIAID NIH HHS AI 43073
6 · The paper itself

Abstract

Myelin/oligodendrocyte glycoprotein (MOG) is a surface-exposed antigen of myelin and an important target for autoimmune responses which mediate inflammatory demyelination in the central nervous system. Experimentally, MOG induces strong pathogenic T cell responses in many strains of laboratory animals. Immunological studies in humans also identify MOG as a surprisingly prevalent antigenic molecule among the myelin proteins. In addition, the encephalitogenic properties of MOG are linked to the induction of antibody responses which have been demonstrated to directly promote central nervous system demyelination, a hallmark neuropathological feature in disorders such as human multiple sclerosis. Factors responsible for autoimmunity to MOG likely include genetic influences as well as other mechanisms, which are the subject of intense investigation. This article reviews experimental data currently available on specificity and pathogenic roles of T cell and antibody responses against MOG, which have implications relevant to multiple sclerosis and related disorders.

Indexed as

Amino Acid SequenceAnimalsAntigens, SurfaceAutoantibodiesAutoantigensB-LymphocytesDemyelinating Autoimmune Diseases, CNSDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalHumansMiceMolecular Sequence DataMultiple SclerosisMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsAntigens, SurfaceAutoantibodiesAutoantigensMOG protein, humanMog protein, mouseMog protein, ratMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin Proteins

Identifiers

PMID11403222
OpenAlexW14049348

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.