Evidence map›Paper›PMID 25946987›Full record

ReviewJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2015

Multiple Sclerosis and T Lymphocytes: An Entangled Story.

Laurine Legroux, Nathalie Arbour

Abstract readReview
In one paragraph

Review in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 1 pooled it
10.6field-weighted citation impact, top 1% 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

101 citing papers in PubMed, 1 synthesis or guideline pooled it, 193 citations in OpenAlex.

  1. Pooled it
  2. Balancing inflammation and regeneration: immune cell dynamics in nerve repair: a comprehensive review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  18. Myelin-reactive B cells exacerbate CD4Nature communications · 2024
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41 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Laurine LegrouxDepartment of Neurosciences, Université de Montréal, CRCHUM Room R09.466, 900 St-Denis, Montréal, QC, Canada, H2X 0A9.
Nathalie ArbourDepartment of Neurosciences, Université de Montréal, CRCHUM Room R09.466, 900 St-Denis, Montréal, QC, Canada, H2X 0A9. nathalie.arbour@umontreal.ca.
Université de Montréal · CA

Funding

CIHR 113558-1
6 · The paper itself

Abstract

Multiple sclerosis (MS) is the prototypic inflammatory disease of the central nervous system (CNS) characterized by multifocal areas of demyelination, axonal damage, activation of glial cells, and immune cell infiltration. Despite intensive years of research, the etiology of this neurological disorder remains elusive. Nevertheless, the abundance of immune cells such as T lymphocytes and their products in CNS lesions of MS patients supports the notion that MS is an immune-mediated disorder. An important body of evidence gathered from MS animal models such as experimental autoimmune encephalomyelitis (EAE), points to the central contribution of CD4 T lymphocytes in disease pathogenesis. Both Th1 (producing interferon-γ) and Th17 (producing interleukin 17) CD4 T lymphocytes targeting CNS self-antigens have been implicated in MS and EAE pathobiology. Moreover, several publications suggest that CD8 T lymphocytes also participate in the development of MS lesions. The migration of activated T lymphocytes from the periphery into the CNS has been identified as a crucial step in the formation of MS lesions. Several factors promote such T cell extravasation including: molecules (e.g., cell adhesion molecules) implicated in the T cell-blood brain barrier interaction, and chemokines produced by neural cells. Finally, once in the CNS, T lymphocytes need to be reactivated by local antigen presenting cells prior to enter the parenchyma where they can initiate damage. Further investigations will be necessary to elucidate the impact of environmental factors (e.g., gut microbiota) and CNS intrinsic properties (e.g., microglial activation) on this inflammatory neurological disease.

Indexed as

AnimalsAutoimmunityCentral Nervous SystemEncephalomyelitis, Autoimmune, ExperimentalHumansMultiple SclerosisT-LymphocytesAutoimmunityCentral nervous systemDemyelinationNeurodegenerationNeuroinflammationT lymphocytes

Identifiers

PMID25946987
PMCPMC5052065
OpenAlexW2097998535

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.