Evidence map›Paper›PMID 38246200›Full record

ArticleBrain research bulletin2024

Tumor necrosis factor receptor 2 activation elicits sex-specific effects on cortical myelin proteins and functional recovery in a model of multiple sclerosis.

Kayla L Nguyen, Ishaan J Bhatt, Shruti Gupta, Nazaf Showkat, Kathryn A Swanson, Roman Fischer, Roland E Kontermann, Klaus Pfizenmaier, Valerie Bracchi-Ricard, John R Bethea

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

Article in Brain research bulletin, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  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
    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

10 authors at 3 institutions in 2 countries.

Kayla L NguyenDepartment of Anatomy and Cell Biology, The George Washington University, Washington, DC 20052, United States. Electronic address: kayla.nguyen@gwu.edu.
Ishaan J BhattDepartment of Biology, Drexel University, Philadelphia, PA 19104, United States.
Shruti GuptaDepartment of Biology, Drexel University, Philadelphia, PA 19104, United States.
Nazaf ShowkatDepartment of Biology, Drexel University, Philadelphia, PA 19104, United States.
Kathryn A SwansonDepartment of Biology, Drexel University, Philadelphia, PA 19104, United States.
Roman FischerInstitute of Cell Biology and Immunology, University of Stuttgart, 70569 Stuttgart, Germany.
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.
Valerie Bracchi-RicardDepartment of Biology, Drexel University, Philadelphia, PA 19104, United States.
John R BetheaDepartment of Anatomy and Cell Biology, The George Washington University, Washington, DC 20052, United States. Electronic address: jrb117@gwu.edu.
Drexel University · USUniversity of Stuttgart · DEGeorge Washington University · US

Funding

TNFR2 Sex Differences and EAER01NS124123 · NINDS · GEORGE WASHINGTON UNIVERSITY · PI John Roland Bethea · 2022 to 2026
$2.0M
NINDS NIH HHS R01 NS124123
6 · The paper itself

Abstract

Multiple sclerosis (MS), a demyelinating autoimmune disease of the central nervous system (CNS), predominately affects females compared to males. Tumor necrosis factor (TNF), a pro-inflammatory cytokine, signaling through TNF receptor 1 contributes to inflammatory disease pathogenesis. In contrast, TNF receptor 2 signaling is neuroprotective. Current anti-TNF MS therapies are shown to be detrimental to patients due to pleiotropic effects on both pro- and anti-inflammatory functions. Using a non-pertussis toxin (nPTX) experimental autoimmune encephalomyelitis (EAE) model in C57BL/6 mice, we systemically administered a TNFR2 agonist (p53-sc-mTNF

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalMultiple SclerosisAnimalsFemaleHumansMaleMiceMice, Inbred C57BLMice, KnockoutMyelin ProteinsReceptors, Tumor Necrosis Factor, Type IITumor Necrosis Factor-alphaTumor Necrosis Factor InhibitorsMyelin ProteinsReceptors, Tumor Necrosis Factor, Type IITumor Necrosis Factor-alphaTumor Necrosis Factor InhibitorsExperimental autoimmune encephalomyelitis (EAE)Multiple sclerosis (MS)Sex differencesTNF receptor 2 (TNFR2)Tumor necrosis factor (TNF)

Identifiers

PMID38246200
PMCPMC10923072
OpenAlexW4391054053

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.