Evidence map›Paper›PMID 30206422›Full record

ArticleScientific reports2018

Anti-TNFR1 targeting in humanized mice ameliorates disease in a model of multiple sclerosis.

Sarah K Williams, Richard Fairless, Olaf Maier, Patricia C Liermann, Kira Pichi, Roman Fischer, Ulrich L M Eisel, Roland Kontermann, Andreas Herrmann, Babette Weksler and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 54 citations in OpenAlex.

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  13. TNF-α Limits Serological Memory by Disrupting the Bone Marrow Niche.Journal of immunology (Baltimore, Md. : 1950) · 2023
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  16. A TNF receptor 2 agonist ameliorates neuropathology and improves cognition in an Alzheimer's disease mouse model.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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 6 institutions in 5 countries.

Sarah K WilliamsDepartment of Neurology, University Clinic Heidelberg, Im Neuenheimer Feld 400, 69120, Heidelberg, Germany. s.williams@dkfz-heidelberg.de.
Richard FairlessDepartment of Neurology, University Clinic Heidelberg, Im Neuenheimer Feld 400, 69120, Heidelberg, Germany.
Olaf MaierInstitute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569, Stuttgart, Germany.
Patricia C LiermannDepartment of Neurology, University Clinic Heidelberg, Im Neuenheimer Feld 400, 69120, Heidelberg, Germany.
Kira PichiDepartment of Neurology, University Clinic Heidelberg, Im Neuenheimer Feld 400, 69120, Heidelberg, Germany.
Roman FischerInstitute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569, Stuttgart, Germany.
Ulrich L M EiselDepartment of Molecular Neurobiology, Groningen Institute of Evolutionary Life Science, Faculty of Science and Engineering, University of Groningen, P.O. Box 11103, NL-9700, CC, Groningen, The Netherlands.ORCID 0000-0003-4178-0384
Roland KontermannInstitute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569, Stuttgart, Germany.
Andreas HerrmannBaliopharm AG, Eulerstr. 55, CH-4051, Basel, Switzerland.
Babette WekslerWeill Medical College of Cornell University, New York, NY, USA.
Nacho RomeroDepartment of Life, Health and Chemical Sciences, The Open University, Milton Keynes, MK7 6AA, UK.
Pierre-Olivier CouraudINSERM, U1016, Institut Cochin, Paris, France.
Klaus PfizenmaierInstitute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569, Stuttgart, Germany.
Ricarda DiemDepartment of Neurology, University Clinic Heidelberg, Im Neuenheimer Feld 400, 69120, Heidelberg, Germany.
Heidelberg University · DEUniversity of Stuttgart · DECornell University · USInserm · FRThe Open University · GBUniversity of Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumour necrosis factor (TNF) signalling is mediated via two receptors, TNF-receptor 1 (TNFR1) and TNF-receptor 2 (TNFR2), which work antithetically to balance CNS immune responses involved in autoimmune diseases such as multiple sclerosis. To determine the therapeutic potential of selectively inhibiting TNFR1 in mice with experimental autoimmune encephalomyelitis, we used chimeric human/mouse TNFR1 knock-in mice allowing the evaluation of antagonistic anti-human TNFR1 antibody efficacy. Treatment of mice after onset of disease with ATROSAB resulted in a robust amelioration of disease severity, correlating with reduced central nervous system immune cell infiltration. Long-term efficacy of treatment was achieved by treatment with the parental mouse anti-human TNFR1 antibody, H398, and extended by subsequent re-treatment of mice following relapse. Our data support the hypothesis that anti-TNFR1 therapy restricts immune cell infiltration across the blood-brain barrier through the down-regulation of TNF-induced adhesion molecules, rather than altering immune cell composition or activity. Collectively, we demonstrate the potential for anti-human TNFR1 therapies to effectively modulate immune responses in autoimmune disease.

Indexed as

AnimalsAntibodies, Monoclonal, Murine-DerivedEncephalomyelitis, Autoimmune, ExperimentalFemaleHumansMiceMice, TransgenicMultiple SclerosisReceptors, Tumor Necrosis Factor, Type IAntibodies, Monoclonal, Murine-DerivedReceptors, Tumor Necrosis Factor, Type ITnfrsf1a protein, mouse

Identifiers

PMID30206422
PMCPMC6133964
OpenAlexW2890730588

What OpenQuestion holds

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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.