Evidence map›Paper›PMID 34305946›Full record

ArticleFrontiers in immunology2021

The TNFR1 Antagonist Atrosimab Is Therapeutic in Mouse Models of Acute and Chronic Inflammation.

Fabian Richter, Sarah K Williams, Katharina John, Carina Huber, Camille Vaslin, Henri Zanker, Richard Fairless, Kira Pichi, Silke Marhenke, Arndt Vogel and 8 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. 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
4.8field-weighted citation impact, top 4% 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, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Is Obesity a Modifiable Risk Factor in Multiple Sclerosis? Mechanistic Insights into Neuroinflammation and Oxidative Damage.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

18 authors at 5 institutions in 1 country.

Fabian RichterInstitute of Cell Biology and Immunology, University of Stuttgart, Stuttgart, Germany.
Sarah K WilliamsDepartment of Neurology, University Clinic Heidelberg, Heidelberg, Germany.
Katharina JohnDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Carina HuberInstitute of Cell Biology and Immunology, University of Stuttgart, Stuttgart, Germany.
Camille VaslinInstitute of Cell Biology and Immunology, University of Stuttgart, Stuttgart, Germany.
Henri ZankerDepartment of Neurology, University Clinic Heidelberg, Heidelberg, Germany.
Richard FairlessDepartment of Neurology, University Clinic Heidelberg, Heidelberg, Germany.
Kira PichiDepartment of Neurology, University Clinic Heidelberg, Heidelberg, Germany.
Silke MarhenkeDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Arndt VogelDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Marie-Ann DhaenBaliopharm, Basel, Switzerland.
Stefanie HerrmannBaliopharm, Basel, Switzerland.
Andreas HerrmannBaliopharm, Basel, Switzerland.
Klaus PfizenmaierInstitute of Cell Biology and Immunology, University of Stuttgart, Stuttgart, Germany.
Heike BantelDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Ricarda DiemDepartment of Neurology, University Clinic Heidelberg, Heidelberg, Germany.
Roland E KontermannInstitute of Cell Biology and Immunology, University of Stuttgart, Stuttgart, Germany.
Roman FischerInstitute of Cell Biology and Immunology, University of Stuttgart, Stuttgart, Germany.
University of Stuttgart · DEMedizinische Hochschule Hannover · DEGerman Cancer Research Center · DEGerman Marine Research Consortium · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Therapeutics that block tumor necrosis factor (TNF), and thus activation of TNF receptor 1 (TNFR1) and TNFR2, are clinically used to treat inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease and psoriasis. However, TNFR1 and TNFR2 work antithetically to balance immune responses involved in inflammatory diseases. In particular, TNFR1 promotes inflammation and tissue degeneration, whereas TNFR2 contributes to immune modulation and tissue regeneration. We, therefore, have developed the monovalent antagonistic anti-TNFR1 antibody derivative Atrosimab to selectively block TNFR1 signaling, while leaving TNFR2 signaling unaffected. Here, we describe that Atrosimab is highly stable at different storage temperatures and demonstrate its therapeutic efficacy in mouse models of acute and chronic inflammation, including experimental arthritis, non-alcoholic steatohepatitis (NASH) and experimental autoimmune encephalomyelitis (EAE). Our data support the hypothesis that it is sufficient to block TNFR1 signaling, while leaving immune modulatory and regenerative responses

Indexed as

AnimalsDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalHumansImmunologic FactorsMiceMice, TransgenicReceptors, Tumor Necrosis Factor, Type ISignal TransductionImmunologic FactorsReceptors, Tumor Necrosis Factor, Type ITNFRSF1A protein, humanTnfrsf1a protein, mousearthritisEAEinflammatory diseasesmultiple sclerosisTNFTNFR1

Identifiers

PMID34305946
PMCPMC8294390
OpenAlexW3177959547

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.