Evidence map›Paper›PMID 25080578›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

CNS repair requires both effector and regulatory T cells with distinct temporal and spatial profiles.

Catarina Raposo, Nadine Graubardt, Merav Cohen, Chen Eitan, Anat London, Tamara Berkutzki, Michal Schwartz

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
9.1field-weighted citation impact, top 2% 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

85 citing papers in PubMed, 158 citations in OpenAlex.

  1. Review
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  5. A Study on Prognostic Risk Factors of Cervical Spondylotic Myelopathy.Journal of Korean Neurosurgical Society · 2025
    Article
  6. Review
  7. Review
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  9. Article
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  11. Article
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  13. Regulatory T lymphocytes in traumatic brain injury.Neurochemistry international · 2024
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

25 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

7 authors at 1 institution in 1 country.

Catarina RaposoDepartment of Neurobiology, Weizmann Institute of Science, 76100 Rehovot, Israel.
Nadine GraubardtDepartment of Neurobiology, Weizmann Institute of Science, 76100 Rehovot, Israel.
Merav CohenDepartment of Neurobiology, Weizmann Institute of Science, 76100 Rehovot, Israel.
Chen EitanDepartment of Neurobiology, Weizmann Institute of Science, 76100 Rehovot, Israel.
Anat LondonDepartment of Neurobiology, Weizmann Institute of Science, 76100 Rehovot, Israel.
Tamara BerkutzkiDepartment of Neurobiology, Weizmann Institute of Science, 76100 Rehovot, Israel.
Michal SchwartzDepartment of Neurobiology, Weizmann Institute of Science, 76100 Rehovot, Israel michal.schwartz@weizmann.ac.il.
Weizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Monocyte-derived macrophages (mo-MΦs) and T cells have been shown to contribute to spinal cord repair. Recently, the remote brain choroid plexus epithelium (CP) was identified as a portal for monocyte recruitment, and its activation for leukocyte trafficking was found to be IFN-γ-dependent. Here, we addressed how the need for effector T cells can be reconciled with the role of inflammation-resolving immune cells in the repair process. Using an acute spinal cord injury model, we show that in mice deficient in IFN-γ-producing T cells, the CP was not activated, and recruitment of inflammation-resolving mo-MΦ to the spinal cord parenchyma was limited. We further demonstrate that mo-MΦ locally regulated recruitment of thymic-derived Foxp3(+) regulatory T (Treg) cells to the injured spinal cord parenchyma at the subacute/chronic phase. Importantly, an ablation protocol that resulted in reduced Tregs at this stage interfered with tissue remodeling, in contrast to Treg transient ablation, restricted to the 4 d period before the injury, which favored repair. The enhanced functional recovery observed following such a controlled decrease of Tregs suggests that reduced systemic immunosuppression at the time of the insult can enhance CNS repair. Overall, our data highlight a dynamic immune cell network needed for repair, acting in discrete compartments and stages, and involving effector and regulatory T cells, interconnected by mo-MΦ. Any of these populations may be detrimental to the repair process if their level or activity become dysregulated. Accordingly, therapeutic interventions must be both temporally and spatially controlled.

Indexed as

AnimalsAntigens, CDCD11c AntigenCX3C Chemokine Receptor 1Diphtheria ToxinDisease Models, AnimalForkhead Transcription FactorsGreen Fluorescent ProteinsHumansMacrophagesMiceMice, Inbred C57BLMice, TransgenicMyelin-Oligodendrocyte GlycoproteinNerve RegenerationPeptide FragmentsAntigens, CDCD11c AntigenCX3C Chemokine Receptor 1Cx3cr1 protein, mouseDiphtheria ToxinForkhead Transcription FactorsFoxp3 protein, mouseGreen Fluorescent ProteinsMyelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide FragmentsReceptors, ChemokineT-Box Domain Protein 2T-Box Domain Proteinsimmune resolutionmonocyte-derived macrophagesspinal cord injuryT cellsTh1Treg

Identifiers

PMID25080578
PMCPMC6608271
OpenAlexW2049161101

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.