Evidence map›Paper›PMID 31220564›Full record

ArticleBrain, behavior, and immunity2019

Exogenous activation of tumor necrosis factor receptor 2 promotes recovery from sensory and motor disease in a model of multiple sclerosis.

Roman Fischer, Tanja Padutsch, Valerie Bracchi-Ricard, Kayla L Murphy, George F Martinez, Niky Delguercio, Nicholas Elmer, Maksim Sendetski, Ricarda Diem, Ulrich L M Eisel and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2019. 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
2.8field-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

28 citing papers in PubMed, 39 citations in OpenAlex.

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  6. Sex-chromosome complement and Activin-A shape the therapeutic potential of TNFR2 activation in a model of MS and CNP.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  16. The role of TNFR2Life sciences · 2021
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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

14 authors at 5 institutions in 3 countries.

Roman FischerDepartment of Biology, Drexel University, Philadelphia, PA 19104, United States. Electronic address: rf428@drexel.edu.
Tanja PadutschDepartment of Biology, Drexel University, Philadelphia, PA 19104, United States.
Valerie Bracchi-RicardDepartment of Biology, Drexel University, Philadelphia, PA 19104, United States.
Kayla L MurphyDepartment of Biology, Drexel University, Philadelphia, PA 19104, United States.
George F MartinezDepartment of Biology, Drexel University, Philadelphia, PA 19104, United States.
Niky DelguercioDepartment of Biology, Drexel University, Philadelphia, PA 19104, United States.
Nicholas ElmerDepartment of Biology, Drexel University, Philadelphia, PA 19104, United States.
Maksim SendetskiDepartment of Biology, Drexel University, Philadelphia, PA 19104, United States.
Ricarda DiemDepartment of Neurology, University Clinic Heidelberg, 69120 Heidelberg, Germany; CCU Neurooncoloy, German Cancer Consortium (DKTK), German Cancer Research Center, Heidelberg, Germany.
Ulrich L M EiselDepartment of Molecular Neurobiology, Groningen Institute for Evolutionary Life Sciences, Faculty of Science and Engineering, University of Groningen, 9747 AG Groningen, Netherlands.
Richard J SmeyneDepartment of Neurosciences, Jefferson Hospital for Neuroscience, Thomas Jefferson University, Philadelphia, PA 19107, United States.
Roland E KontermannInstitute of Cell Biology and Immunology, University of Stuttgart, 70569 Stuttgart, Germany; Stuttgart Research Center Systems Biology, University of Stuttgart, 70569 Stuttgart, Germany.
Klaus PfizenmaierInstitute of Cell Biology and Immunology, University of Stuttgart, 70569 Stuttgart, Germany; Stuttgart Research Center Systems Biology, University of Stuttgart, 70569 Stuttgart, Germany.
John R BetheaDepartment of Biology, Drexel University, Philadelphia, PA 19104, United States. Electronic address: jrb445@drexel.edu.
Drexel University · USUniversity of Stuttgart · DEJefferson Hospital for Neuroscience · USUniversity Hospital Heidelberg · DEUniversity of Groningen · NL

Funding

TNF in Injury and Repair Processes Following Traumatic SCIR01NS051709 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI John Roland Bethea · 2005 to 2026
$8.0M
NINDS NIH HHS R01 NS051709
6 · The paper itself

Abstract

Tumor necrosis factor receptor 2 (TNFR2) is a transmembrane receptor that promotes immune modulation and tissue regeneration and is recognized as a potential therapeutic target for multiple sclerosis (MS). However, TNFR2 also contributes to T effector cell function and macrophage-TNFR2 recently was shown to promote disease development in the experimental autoimmune encephalomyelitis (EAE) model of MS. We here demonstrate that systemic administration of a TNFR2 agonist alleviates peripheral and central inflammation, and reduces demyelination and neurodegeneration, indicating that protective signals induced by TNFR2 exceed potential pathogenic TNFR2-dependent responses. Our behavioral data show that systemic treatment of female EAE mice with a TNFR2 agonist is therapeutic on motor symptoms and promotes long-term recovery from neuropathic pain. Mechanistically, our data indicate that TNFR2 agonist treatment follows a dual mode of action and promotes both suppression of CNS autoimmunity and remyelination. Strategies based on the concept of exogenous activation of TNFR2 therefore hold great promise as a new therapeutic approach to treat motor and sensory disease in MS as well as other inflammatory diseases or neuropathic pain conditions.

Indexed as

AnimalsAutoimmunityDemyelinating DiseasesEncephalomyelitis, Autoimmune, ExperimentalFemaleInflammationMacrophagesMiceMice, Inbred C57BLMultiple SclerosisNeuralgiaNeurodegenerative DiseasesReceptors, Tumor Necrosis Factor, Type IISpinal CordT-Lymphocytes, RegulatoryTumor Necrosis Factor-alphaReceptors, Tumor Necrosis Factor, Type IITumor Necrosis Factor-alphaEAEPainRecoveryTNFTNFR2

Identifiers

PMID31220564
PMCPMC6754799
OpenAlexW2951700136

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.