Evidence map›Paper›PMID 37122019›Full record

ArticleJournal of neuroinflammation2023

Co-modulation of TNFR1 and TNFR2 in an animal model of multiple sclerosis.

Timon Fiedler, Richard Fairless, Kira Pichi, Roman Fischer, Fabian Richter, Roland E Kontermann, Klaus Pfizenmaier, Ricarda Diem, Sarah K Williams

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
7.7field-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

18 citing papers in PubMed, 30 citations in OpenAlex.

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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

9 authors at 6 institutions in 1 country.

Timon Fiedler *Department of Neurology, University Clinic Heidelberg, University of Heidelberg, Otto-Mayerhof-Zentrum (OMZ), Im Neuenheimer Feld 350, 69120, Heidelberg, Germany.
Richard Fairless *Department of Neurology, University Clinic Heidelberg, University of Heidelberg, Otto-Mayerhof-Zentrum (OMZ), Im Neuenheimer Feld 350, 69120, Heidelberg, Germany.
Kira PichiDepartment of Neurology, University Clinic Heidelberg, University of Heidelberg, Otto-Mayerhof-Zentrum (OMZ), Im Neuenheimer Feld 350, 69120, Heidelberg, Germany.
Roman FischerInstitute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569, Stuttgart, Germany.
Fabian RichterInstitute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569, Stuttgart, Germany.
Roland E KontermannInstitute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569, Stuttgart, Germany.
Klaus PfizenmaierInstitute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569, Stuttgart, Germany.
Ricarda DiemDepartment of Neurology, University Clinic Heidelberg, University of Heidelberg, Otto-Mayerhof-Zentrum (OMZ), Im Neuenheimer Feld 350, 69120, Heidelberg, Germany.
Sarah K WilliamsDepartment of Neurology, University Clinic Heidelberg, University of Heidelberg, Otto-Mayerhof-Zentrum (OMZ), Im Neuenheimer Feld 350, 69120, Heidelberg, Germany. s.williams@Dkfz-heidelberg.de.
University Hospital Heidelberg · DEUniversity of Stuttgart · DEBioNTech (Germany) · DEGerman Cancer Research Center · DEHeidelberg University · DEImmatics Biotechnologies (Germany) · DE

Funding

Deutsche Forschungsgemeinschaft FOR2289
6 · The paper itself

Abstract

backgroundTumour necrosis factor (TNF) is a pleiotropic cytokine and master regulator of the immune system. It acts through two receptors resulting in often opposing biological effects, which may explain the lack of therapeutic potential obtained so far in multiple sclerosis (MS) with non-receptor-specific anti-TNF therapeutics. Under neuroinflammatory conditions, such as MS, TNF receptor-1 (TNFR1) is believed to mediate the pro-inflammatory activities associated with TNF, whereas TNF receptor-2 (TNFR2) may instead induce anti-inflammatory effects as well as promote remyelination and neuroprotection. In this study, we have investigated the therapeutic potential of blocking TNFR1 whilst simultaneously stimulating TNFR2 in a mouse model of MS.

methodsExperimental autoimmune encephalomyelitis (EAE) was induced with myelin oligodendrocyte glycoprotein (MOG

resultsTNFR modulation successfully ameliorated symptoms of EAE and reduced demyelination, inflammatory infiltration and axonal degeneration. Furthermore, the combinatorial approach of blocking TNFR1 and stimulating TNFR2 signalling increased RGC survival and promoted the phosphorylation of Akt and NF-κB, both known to mediate neuroprotection.

conclusionThese results further support the potential of regulating the balance of TNFR signalling, through the co-modulation of TNFR1 and TNFR2 activity, as a novel therapeutic approach in treating inflammatory demyelinating disease.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalMultiple SclerosisAnimalsAntibodiesHumansMiceReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IITumor Necrosis Factor-alphaTumor Necrosis Factor InhibitorsAntibodiesReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IITumor Necrosis Factor-alphaTumor Necrosis Factor InhibitorsEAENeuroinflammationNeuroprotectionTNFR1TNFR2

Identifiers

PMID37122019
PMCPMC10149004
OpenAlexW4367557647

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.