Evidence map›Paper›PMID 29491183›Full record

ArticleScience translational medicine2018

Fast direct neuronal signaling via the IL-4 receptor as therapeutic target in neuroinflammation.

Christina F Vogelaar, Shibajee Mandal, Steffen Lerch, Katharina Birkner, Jerome Birkenstock, Ulrike Bühler, Andrea Schnatz, Cedric S Raine, Stefan Bittner, Johannes Vogt and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Science translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 82 citations in OpenAlex.

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  17. The neuropathobiology of multiple sclerosis.Nature reviews. Neuroscience · 2024
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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

13 authors at 3 institutions in 2 countries.

Christina F VogelaarDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.ORCID 0000-0002-9683-7336
Shibajee MandalDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.ORCID 0000-0002-6112-6972
Steffen LerchDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.ORCID 0000-0002-4752-0498
Katharina BirknerDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.ORCID 0000-0002-8650-7819
Jerome BirkenstockDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.ORCID 0000-0002-3418-9847
Ulrike BühlerDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.
Andrea SchnatzInstitute for Microanatomy and Neurobiology, Focus Program Translational Neuroscience (FTN), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.ORCID 0000-0003-4855-8663
Cedric S RaineNeuropathology, Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.ORCID 0000-0001-9567-1963
Stefan BittnerDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.
Johannes VogtInstitute for Microanatomy and Neurobiology, Focus Program Translational Neuroscience (FTN), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.ORCID 0000-0003-2439-8247
Jonathan KipnisGutenberg Research Fellowship Group of Neuroimmunology, Focus Program Translational Neuroscience (FTN) and Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.
Robert NitschInstitute for Translational Neuroscience, University Medical Center, Westfälische Wilhelms-University Münster, Albert-Schweitzer-Campus, 48149 Münster, Germany.
Frauke ZippDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany. frauke.zipp@unimedizin-mainz.de.ORCID 0000-0002-1231-1928
Johannes Gutenberg University Mainz · DEAlbert Einstein College of Medicine · USUniversity of Münster · DE

Funding

Immune Response to CNS InjuryR01NS096967 · NINDS · WASHINGTON UNIVERSITY · PI KIPNIS, JONATHAN · 2016 to 2020
$1.7M
NINDS NIH HHS R01 NS096967
6 · The paper itself

Abstract

Ongoing axonal degeneration is thought to underlie disability in chronic neuroinflammation, such as multiple sclerosis (MS), especially during its progressive phase. Upon inflammatory attack, axons undergo pathological swelling, which can be reversible. Because we had evidence for beneficial effects of T helper 2 lymphocytes in experimental neurotrauma and discovered interleukin-4 receptor (IL-4R) expressed on axons in MS lesions, we aimed at unraveling the effects of IL-4 on neuroinflammatory axon injury. We demonstrate that intrathecal IL-4 treatment during the chronic phase of several experimental autoimmune encephalomyelitis models reversed disease progression without affecting inflammation. Amelioration of disability was abrogated upon neuronal deletion of IL-4R. We discovered direct neuronal signaling via the IRS1-PI3K-PKC pathway underlying cytoskeletal remodeling and axonal repair. Nasal IL-4 application, suitable for clinical translation, was equally effective in improving clinical outcome. Targeting neuronal IL-4 signaling may offer new therapeutic strategies to halt disability progression in MS and possibly also neurodegenerative conditions.

Indexed as

Administration, IntranasalAnimalsAxonsEncephalomyelitis, Autoimmune, ExperimentalHumansInflammationInterleukin-4LocomotionMaleMiceMultiple SclerosisNeuronsReceptors, Interleukin-4Interleukin-4Receptors, Interleukin-4

Identifiers

PMID29491183
PMCPMC12102061
OpenAlexW2788475922

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.