Evidence map›Paper›PMID 19841745›Full record

ArticlePLoS medicine2009

Potential role of decoy B7-H4 in the pathogenesis of rheumatoid arthritis: a mouse model informed by clinical data.

Takeshi Azuma, Gefeng Zhu, Haiying Xu, A Cecilia Rietz, Charles G Drake, Eric L Matteson, Lieping Chen

Open access · goldAbstract read
In one paragraph

Article in PLoS medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

38 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. B7-DC (PD-L2) costimulation of CD4Cellular & molecular immunology · 2018
    Article
  14. Article
  15. B7-H4 Modulates Regulatory CD4Journal of immunology (Baltimore, Md. : 1950) · 2018
    Article
  16. Review
  17. Article
  18. Article
  19. New B7 Family Checkpoints in Human Cancers.Molecular cancer therapeutics · 2017
    Review
  20. Review
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 3 institutions in 1 country.

Takeshi AzumaDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Gefeng Zhu
Haiying Xu
A Cecilia Rietz
Charles G Drake
Eric L Matteson
Lieping Chen
Johns Hopkins Medicine · USJohns Hopkins University · USMayo Clinic · US

Funding

Therapeutic Manipulation of the B7-like MoleculesR01CA098731 · NCI · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI CHEN, LIEPING · 2003 to 2007
$1.7M
NCI NIH HHS CA98731NCI NIH HHS R01 CA098731
6 · The paper itself

Abstract

backgroundA pathogenic hallmark of rheumatoid arthritis (RA) is persistent inflammatory responses in target tissues and organs. Immune responses mediated by T cells and autoantibodies are known to play pivotal roles. A possible interpretation for this observation is a loss of negative regulation of autoimmune responses. Here we sought to investigate whether B7-H4, a cell surface inhibitory molecule of the B7-CD28 signaling pathway, may play a role in the pathogenesis of RA. METHODS AND

findingsIn a cross-sectional study of a clinical convenience sample using monoclonal antibodies against human B7-H4 molecules, we detected high levels of the soluble form of B7-H4 (sH4) in the sera of 65% of patients with RA (n = 68) versus only 13% of healthy donors (n = 24). Elevated sH4 was associated with an increased disease severity score (DAS28) in a cross-sectional analysis. In a mouse model of RA, transgenic expression of sH4 or genetic deletion of B7-H4 accelerated the progression of collagen-induced arthritis, accompanied by enhanced T and B cell-mediated autoimmune responses as well as increased activity of neutrophils. Expression in vivo of an agonist, a B7-H4-immunoglobulin Fc fusion protein, profoundly suppressed disease progression in the mouse model.

conclusionsOur findings in mice indicate that sH4 acts as a decoy molecule to block the inhibitory functions of cell-surface B7-H4, leading to exacerbation of collagen-induced arthritis. If the preliminary correlation between sH4 levels and disease activity in patients with RA can be confirmed to reflect a similar mechanism, these findings suggest a novel target for treatment approaches. Please see later in the article for the Editors' Summary.

Indexed as

AnimalsAntibodies, MonoclonalArthritis, RheumatoidB7-1 AntigenCross-Sectional StudiesHumansMaleMiceMice, Inbred DBAModels, AnimalV-Set Domain-Containing T-Cell Activation Inhibitor 1Antibodies, MonoclonalB7-1 AntigenV-Set Domain-Containing T-Cell Activation Inhibitor 1VTCN1 protein, human

Identifiers

PMID19841745
PMCPMC2760136
OpenAlexW2021181739

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.