Evidence map›Paper›PMID 11583948›Full record

ArticleThe American journal of pathology2001

In vivo expression of major histocompatibility complex molecules on oligodendrocytes and neurons during viral infection.

J M Redwine, M J Buchmeier, C F Evans

Abstract read
In one paragraph

Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
–field-weighted citation impact
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

53 citing papers in PubMed.

  1. Review
  2. Getting on your last nerve: IFNs and resistance to infection.Journal of immunology (Baltimore, Md. : 1950) · 2026
    Review
  3. Immune cell profiling reveals expanded stem cell-like memory T cells in anti-GAD65-associated neurological syndromes.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Brain communications · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Pro-inflammatory T helper 17 directly harms oligodendrocytes in neuroinflammation.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  11. Review
  12. Promoting remyelination through cell transplantation therapies in a model of viral-induced neurodegenerative disease.Developmental dynamics : an official publication of the American Association of Anatomists · 2019
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  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

3 authors.

J M RedwineDepartment of Neuropharmacology, The Scripps Research Institute, La Jolla, California, USA.
M J Buchmeier
C F Evans

Funding

CONTROL OF MHV INFECTION IN THE CENTRAL NERVOUS SYSTEMR01AI043103 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI BUCHMEIER, MICHAEL · 1998 to 2002
$862k
NEUROBIOLOGIC AND IMMUNOLOGIC ASPECTS OF AGINGT32AG000080 · NIA · SCRIPPS RESEARCH INSTITUTE · PI BUXBAUM, JOEL N · 1985 to 2003
$743k
STUDIES OF A NEW MYELIN GENE THAT CAUSES CNS DISEASER01NS038719 · NINDS · SCRIPPS RESEARCH INSTITUTE · PI OLDSTONE, MICHAEL B · 1999 to 2001
$572k
IFN GAMMA--ROLES IN DEMYELINATION AND AUTOIMMUNITYR29NS037135 · NINDS · SCRIPPS RESEARCH INSTITUTE · PI EVANS, CLAIRE FRANCES · 1998 to 2000
$123k
NIAID NIH HHS AI43103NIA NIH HHS 5T32 AG00080-21NIA NIH HHS T32 AG000080NINDS NIH HHS NS37135NINDS NIH HHS NS38719
6 · The paper itself

Abstract

Demyelination in multiple sclerosis and in animal models is associated with infiltrating CD8+ and CD4+ T cells. Although oligodendrocytes and axons are damaged in these diseases, the roles T cells play in the demyelination process are not completely understood. Antigen-specific CD8+ T cell lysis of target cells is dependent on interactions between the T cell receptor and major histocompatibility complex (MHC) class I-peptide complexes on the target cell. In the normal central nervous system, expression of MHC molecules is very low but often increases during inflammation. We set out to precisely define which central nervous system cells express MHC molecules in vivo during infection with a strain of murine hepatitis virus that causes a chronic, inflammatory demyelinating disease. Using double immunofluorescence labeling, we show that during acute infection with murine hepatitis virus, MHC class I is expressed in vivo by oligodendrocytes, neurons, microglia, and endothelia, and MHC class II is expressed only by microglia. These data indicate that oligodendrocytes and neurons have the potential to present antigen to T cells and thus be damaged by direct antigen-specific interactions with CD8+ T lymphocytes.

Indexed as

Murine hepatitis virusAnimalsCoronavirus InfectionsDemyelinating DiseasesEndothelium, VascularFemaleGenetic VariationHistocompatibility Antigens Class IHistocompatibility Antigens Class IIMaleMiceMice, Inbred BALB CMicrogliaNeuronsOligodendrogliaSpinal Cord DiseasesHistocompatibility Antigens Class IHistocompatibility Antigens Class II

Identifiers

PMID11583948
PMCPMC1850521

What OpenQuestion holds

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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.