Evidence map›Paper›PMID 19279679›Full record

ArticlePloS one2009

Molecular blocking of CD23 supports its role in the pathogenesis of arthritis.

Jérôme Rambert, Maria Mamani-Matsuda, Daniel Moynet, Pierre Dubus, Vanessa Desplat, Tina Kauss, Joël Dehais, Thierry Schaeverbeke, Khaled Ezzedine, Denis Malvy and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Trial
  2. Fungi, host immune response, and tumorigenesis.American journal of physiology. Gastrointestinal and liver physiology · 2021
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. CD23/FcεRII: molecular multi-tasking.Clinical and experimental immunology · 2010
    Review
  10. Article
  11. Article
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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

12 authors at 2 institutions in 1 country.

Jérôme RambertGroupe Thérapeutiques d'inflammation et d'infection, Laboratoire d'Immunologie et de Parasitologie, UFR Sciences Pharmaceutiques, Université Bordeaux 2, Bordeaux, France.
Maria Mamani-Matsuda
Daniel Moynet
Pierre Dubus
Vanessa Desplat
Tina Kauss
Joël Dehais
Thierry Schaeverbeke
Khaled Ezzedine
Denis Malvy
Philippe Vincendeau
M Djavad Mossalayi
Hôpital Pellegrin · FRUniversité de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCD23 is a differentiation/activation antigen expressed by a variety of hematopoietic and epithelial cells. It can also be detected in soluble forms in biological fluids. Initially known as the low-affinity receptor for immunoglobulin E (Fc epsilonRII), CD23 displays various other physiologic ligands such as CD21, CD11b/c, CD47-vitronectin, and mannose-containing proteins. CD23 mediates numerous immune responses by enhancing IgE-specific antigen presentation, regulating IgE synthesis, influencing cell differentiation and growth of both B- and T-cells. CD23-crosslinking promotes the secretion of pro-inflammatory mediators from human monocytes/macrophages, eosinophils and epithelial cells. Increased CD23 expression is found in patients during allergic reactions and rheumatoid arthritis while its physiopathologic role in these diseases remains to be clarified. METHODOLOGY/PRINCIPAL

findingsWe previously generated heptapeptidic countrestructures of human CD23. Based on in vitro studies on healthy and arthritic patients' cells, we showed that CD23-specific peptide addition to human macrophages greatly diminished the transcription of genes encoding inflammatory cytokines. This was also confirmed by significant reduction of mediator levels in cell supernatants. We also show that CD23 peptide decreased IgE-mediated activation of both human and rat CD23(+) macrophages. In vivo studies in rat model of arthritis showed that CD23-blocking peptide ameliorates clinical scores and prevent bone destruction in a dose dependent manner. Ex-vivo analysis of rat macrophages further confirmed the inhibitory effect of peptides on their activation. Taken together our results support the role of CD23 activation and subsequent inflammatory response in arthritis.

conclusionCD23-blocking peptide (p30A) prevents the activation of monocytes/macrophages without cell toxicity. Thus, targeting CD23 by antagonistic peptide decreases inflammatory markers and may have clinical value in the treatment of human arthritis and allergic reactions involving CD23.

Indexed as

AnimalsArthritisBase SequenceBlotting, WesternCase-Control StudiesDNA PrimersFemaleHumansMacrophages, PeritonealRatsRats, Inbred LewReceptors, IgESignal TransductionDNA PrimersReceptors, IgE

Identifiers

PMID19279679
PMCPMC2652713
OpenAlexW1994387933

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.