Evidence map›Paper›PMID 11748282›Full record

ArticleThe Journal of experimental medicine2001

The extracellular domain of CD83 inhibits dendritic cell-mediated T cell stimulation and binds to a ligand on dendritic cells.

M Lechmann, D J Krooshoop, D Dudziak, E Kremmer, C Kuhnt, C G Figdor, G Schuler, A Steinkasserer

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

60 citing papers in PubMed, 190 citations in OpenAlex.

  1. Article
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  5. Review
  6. CD83 Regulates the Immune Responses in Inflammatory Disorders.International journal of molecular sciences · 2023
    Review
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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

8 authors at 2 institutions in 2 countries.

M LechmannDepartment of Dermatology, University of Erlangen-Nuremberg, D-91052 Erlangen, Germany.
D J Krooshoop
D Dudziak
E Kremmer
C Kuhnt
C G Figdor
G Schuler
A Steinkasserer
Friedrich-Alexander-Universität Erlangen-Nürnberg · DERadboud University Nijmegen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD83 is an immunoglobulin (Ig) superfamily member that is upregulated during the maturation of dendritic cells (DCs). It has been widely used as a marker for mature DCs, but its function is still unknown. To approach its potential functional role, we have expressed the extracellular Ig domain of human CD83 (hCD83ext) as a soluble protein. Using this tool we could show that immature as well as mature DCs bind to CD83. Since CD83 binds a ligand also expressed on immature DCs, which do not express CD83, indicates that binding is not a homophilic interaction. In addition we demonstrate that hCD83ext interferes with DC maturation downmodulating the expression of CD80 and CD83, while no phenotypical effects were observed on T cells. Finally, we show that hCD83ext inhibits DC-dependent allogeneic and peptide-specific T cell proliferation in a concentration dependent manner in vitro. This is the first report regarding functional aspects of CD83 and the binding of CD83 to DCs.

Indexed as

Antigen PresentationAntigens, CDCD83 AntigenCell CommunicationCell DifferentiationCells, CulturedDendritic CellsEscherichia coliHumansImmunoglobulin FragmentsImmunoglobulinsLigandsMembrane GlycoproteinsProtein BindingT-LymphocytesAntigens, CDCD83 AntigenImmunoglobulin FragmentsImmunoglobulinsLigandsMembrane Glycoproteins

Identifiers

PMID11748282
PMCPMC2193570
OpenAlexW2134246923

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.