Evidence map›Paper›PMID 31693930›Full record

ReviewNeuroscience letters2020

Immune cell modulation of oligodendrocyte lineage cells.

Emily P Harrington, Dwight E Bergles, Peter A Calabresi

Open access · greenAbstract readReview
In one paragraph

Review in Neuroscience letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

41 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. The Many Lives of an Oligodendrocyte Precursor Cell.Annual review of neuroscience · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Demyelination and impaired oligodendrogenesis in the corpus callosum following lead exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2024
    Article
  14. Review
  15. NKG2C/Journal for immunotherapy of cancer · 2024
    Article
  16. Article
  17. Review
  18. Review
  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

3 authors at 1 institution in 1 country.

Emily P HarringtonDepartment of Neurology, Johns Hopkins University School of Medicine, 600 N. Wolfe St., Pathology 509, Baltimore, MD, 21287, USA; The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, 725 N. Wolfe St., WBSB 1001, Baltimore, MD, 21205, USA.
Dwight E BerglesThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, 725 N. Wolfe St., WBSB 1001, Baltimore, MD, 21205, USA; The Kavli Neuroscience Discovery Institute, Johns Hopkins University, Baltimore, MD, USA.
Peter A CalabresiDepartment of Neurology, Johns Hopkins University School of Medicine, 600 N. Wolfe St., Pathology 509, Baltimore, MD, 21287, USA; The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, 725 N. Wolfe St., WBSB 1001, Baltimore, MD, 21205, USA. Electronic address: Calabresi@jhmi.edu.
Johns Hopkins University · US

Funding

The Role of KV1.3 in Effector T cellsR01NS041435 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI CALABRESI, PETER A · 2000 to 2025
$5.8M
Mechanisms by which effector T cells modulate endogenous remyelinationR37NS041435 · NINDS · JOHNS HOPKINS UNIVERSITY · PI CALABRESI, PETER A · 2013 to 2019
$3.0M
NINDS NIH HHS R01 NS041435NINDS NIH HHS R37 NS041435
6 · The paper itself

Abstract

Chronic demyelination and the concomitant loss of trophic support and increased energy demands in axons are thought to contribute to neurodegeneration in a number of neurological diseases such as multiple sclerosis (MS). Adult oligodendrocyte precursor cells (OPCs) play an important role in these demyelinating diseases by generating new myelinating oligodendrocytes that may help limit axonal degeneration. Thus, promoting the differentiation of OPCs and functional integration of newly generated oligodendrocytes is a crucial avenue for the next generation of therapies. Evidence to date suggests that the immune system may both positively and negatively impact OPC differentiation and endogenous remyelination in disease. Inflammatory cytokines not only suppress OPC differentiation but may also directly affect other functions of OPCs. Recent studies have demonstrated that OPCs and oligodendrocytes in both human multiple sclerosis lesions and mouse models of demyelination can express an immunogenic transcriptional signature and upregulate antigen presenting genes. In inflammatory demyelinating mouse models OPCs are capable of presenting antigen and activating CD8 + T cells. Here we review the evidence for this new role of oligodendroglia as antigen presenting cells and how these inflammatory OPCs (iOPCs) and inflammatory oligodendrocytes (iOLs) may influence myelin repair and other disease processes.

Indexed as

AnimalsCell LineageCytokinesHumansImmunity, CellularMicrogliaOligodendrogliaT-LymphocytesCytokinesAntigen presentationCD8 T cellsMultiple sclerosisMyelin repairOligodendrocytesRemyelination

Identifiers

PMID31693930
PMCPMC6981227
OpenAlexW2983265482

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.