Evidence map›Paper›PMID 26193120›Full record

ArticleeLife2015

A pain-mediated neural signal induces relapse in murine autoimmune encephalomyelitis, a multiple sclerosis model.

Yasunobu Arima, Daisuke Kamimura, Toru Atsumi, Masaya Harada, Tadafumi Kawamoto, Naoki Nishikawa, Andrea Stofkova, Takuto Ohki, Kotaro Higuchi, Yuji Morimoto and 11 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.1field-weighted citation impact, top 7% 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, 64 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. IL-6 in inflammation, autoimmunity and cancer.International immunology · 2021
    Review
  16. Gateway Reflex and Mechanotransduction.Frontiers in immunology · 2021
    Review
  17. Review
  18. Article
  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

21 authors at 8 institutions in 2 countries.

Yasunobu ArimaDivision of Molecular Neuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Daisuke KamimuraDivision of Molecular Neuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Toru AtsumiDivision of Molecular Neuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Masaya HaradaDivision of Molecular Neuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Tadafumi KawamotoDepartment of Dentistry, Tsurumi University, Yokohama, Japan.
Naoki NishikawaDivision of Molecular Neuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Andrea StofkovaDivision of Molecular Neuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Takuto OhkiDivision of Molecular Neuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Kotaro HiguchiDivision of Molecular Neuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Yuji MorimotoDepartment of Anesthesiology and Critical Care Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Peter WieghoferInstitute of Neuropathology, Faculty of Biology, University of Freiburg, Freiburg, Germany.
Yuka OkadaDepartment of Ophthalmology, Wakayama Medical University, Wakayama, Japan.
Yuki MoriLaboratory of Biofunctional Imaging, WPI Immunology Frontier Research Center, Osaka University, Osaka, Japan.
Saburo SakodaDepartment of Neurology, National Hospital Organization Toneyama Hospital, Osaka, Japan.
Shizuya SaikaDepartment of Ophthalmology, Wakayama Medical University, Wakayama, Japan.
Yoshichika YoshiokaLaboratory of Biofunctional Imaging, WPI Immunology Frontier Research Center, Osaka University, Osaka, Japan.
Issei KomuroDepartment of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Toshihide YamashitaLaboratory of Molecular Neuroscience, Graduate School of Medicine, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan.
Toshio HiranoOsaka University, Osaka, Japan.
Marco PrinzBIOSS Centre for Biological Signalling Studies, University of Freiburg, Freiburg, Germany.
Masaaki MurakamiDivision of Molecular Neuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Osaka University · JPHokkaido University · JPUbe Frontier University · JPUniversity of Freiburg · DEWakayama Medical University · JPThe University of Tokyo · JPToneyama National Hospital · JPTsurumi University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although pain is a common symptom of various diseases and disorders, its contribution to disease pathogenesis is not well understood. Here we show using murine experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis (MS), that pain induces EAE relapse. Mechanistic analysis showed that pain induction activates a sensory-sympathetic signal followed by a chemokine-mediated accumulation of MHC class II+CD11b+ cells that showed antigen-presentation activity at specific ventral vessels in the fifth lumbar cord of EAE-recovered mice. Following this accumulation, various immune cells including pathogenic CD4+ T cells recruited in the spinal cord in a manner dependent on a local chemokine inducer in endothelial cells, resulting in EAE relapse. Our results demonstrate that a pain-mediated neural signal can be transformed into an inflammation reaction at specific vessels to induce disease relapse, thus making this signal a potential therapeutic target.

Indexed as

PainAnimalsAntigen-Presenting CellsCD4-Positive T-LymphocytesChemokinesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalMiceMultiple SclerosisRecurrenceSpinal CordChemokinesCD4 T cell-mediated diseaseEAEimmunologymouseneural signalingrelapse

Identifiers

PMID26193120
PMCPMC4530187
OpenAlexW1836377684

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.