Evidence map›Paper›PMID 21666956›Full record

ArticleMolecular medicine (Cambridge, Mass.)

Monoclonal anti-HMGB1 (high mobility group box chromosomal protein 1) antibody protection in two experimental arthritis models.

Hanna Schierbeck, Peter Lundbäck, Karin Palmblad, Lena Klevenvall, Helena Erlandsson-Harris, Ulf Andersson, Lars Ottosson

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
7.1field-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

67 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
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  10. The Role of Alarmins in Osteoarthritis Pathogenesis: HMGB1, S100B and IL-33.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. The Role of HMGB1 in Rheumatic Diseases.Frontiers in immunology · 2022
    Review
  16. HMGB-1 in Psoriasis.Biomolecules · 2021
    Article
  17. Article
  18. HMGB1 as a therapeutic target in disease.Journal of cellular physiology · 2021
    Review
  19. Review
  20. Article

7 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Hanna SchierbeckDepartment of Women's and Children's Health, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Peter Lundbäck
Karin Palmblad
Lena Klevenvall
Helena Erlandsson-Harris
Ulf Andersson
Lars Ottosson
Karolinska University Hospital · SEKarolinska Institutet · SE

Funding

Medical Research Council
6 · The paper itself

Abstract

High mobility group box chromosomal protein 1 (HMGB1) is a DNA-binding nuclear protein that can be released from dying cells and activated myeloid cells. Extracellularly, HMGB1 promotes inflammation. Experimental studies demonstrate HMGB1 to be a pathogenic factor in many inflammatory conditions including arthritis. HMGB1-blocking therapies in arthritis models alleviate disease and confer significant protection against cartilage and bone destruction. So far, the most successful HMGB1-targeted therapies have been demonstrated with HMGB1-specific polyclonal antibodies and with recombinant A box protein, a fragment of HMGB1. The present study is the first to evaluate the potential of a monoclonal anti-HMGB1 antibody (2G7, mouse IgG2b) to ameliorate arthritis. Effects of repeated injections of this antibody have now been studied in two conceptually different models of arthritis: collagen type II-induced arthritis (CIA) in DBA/1 mice and in a spontaneous arthritis disease in mice with combined deficiencies for genes encoding for the enzyme DNase type II and interferon type I receptors. These mice are unable to degrade phagocytozed DNA in macrophages and develop chronic, destructive polyarthritis. Therapeutic intervention in CIA and prophylactic administration of anti-HMGB1 monoclonal antibody (mAb) in the spontaneous arthritis model significantly ameliorated the clinical courses. Anti-HMGB1 mAb therapy also partially prevented joint destruction, as demonstrated by histological examination. The beneficial antiarthritic effects by the anti-HMGB1 mAb in two diverse models of arthritis represent additional proof-of-concept, indicating that HMGB1 may be a valid target molecule to consider for development of future clinical therapy.

Indexed as

AnimalsAnkle JointAntibodies, MonoclonalArthritis, ExperimentalCollagen Type IIEndodeoxyribonucleasesFemaleHMGB1 ProteinJointsMaleMetacarpophalangeal JointMetatarsophalangeal JointMiceMice, Inbred DBAMice, KnockoutReceptor, Interferon alpha-betaAntibodies, MonoclonalCollagen Type IIdeoxyribonuclease IIEndodeoxyribonucleasesHMGB1 ProteinReceptor, Interferon alpha-beta

Identifiers

PMID21666956
PMCPMC3188862
OpenAlexW2206714426

What OpenQuestion holds

Textmetadata
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.