Evidence map›Paper›PMID 24424524›Full record

ArticleMucosal immunology2014

Soluble CD83 ameliorates experimental colitis in mice.

J Eckhardt, S Kreiser, M Döbbeler, C Nicolette, M A DeBenedette, I Y Tcherepanova, C Ostalecki, A J Pommer, C Becker, C Günther and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. CD83 Regulates the Immune Responses in Inflammatory Disorders.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Article
  8. Cells · 2022
    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

14 authors at 3 institutions in 3 countries.

J EckhardtDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
S KreiserDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
M DöbbelerDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
C NicoletteArgos Therapeutics, Durham, North Carolina, USA.
M A DeBenedetteArgos Therapeutics, Durham, North Carolina, USA.
I Y TcherepanovaArgos Therapeutics, Durham, North Carolina, USA.
C OstaleckiDepartment of Dermatology, University Hospital Erlangen, Erlangen, Germany.
A J PommerDepartment of Dermatology, University Hospital Erlangen, Erlangen, Germany.
C BeckerDepartment of Medicine 1, University Hospital Erlangen, Erlangen, Germany.
C GüntherDepartment of Medicine 1, University Hospital Erlangen, Erlangen, Germany.
E ZinserDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
T W MakThe Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada.
A SteinkassererDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
M LechmannDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
Universitätsklinikum Erlangen · DEArgos Therapeutics (United States) · USPrincess Margaret Cancer Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The physiological balance between pro- and anti-inflammatory processes is dysregulated in inflammatory bowel diseases (IBD) as in Crohn's disease and ulcerative colitis. Conventional therapy uses anti-inflammatory and immunosuppressive corticosteroids to treat acute-phase symptoms. However, low remission rate and strong side effects of these therapies are not satisfying. Thus, there is a high medical need for new therapeutic strategies. Soluble CD83, the extracellular domain of the transmembrane CD83 molecule, has been reported to have interesting therapeutic and immunosuppressive properties by suppressing dendritic cell (DC)-mediated T-cell activation and inducing tolerogenic DCs. However, the expression and function of CD83 in IBD is still unknown. Here, we show that CD83 expression is upregulated by different leukocyte populations in a chemical-induced murine colitis model. Furthermore, in this study the potential of sCD83 to modulate colitis using an experimental murine colitis model was investigated. Strikingly, sCD83 ameliorated the clinical disease symptoms, drastically reduced mortality, and strongly decreased inflammatory cytokine expression in mesenteric lymph nodes and colon. The infiltration of macrophages and granulocytes into colonic tissues was vigorously inhibited. Mechanistically, we could show that sCD83-induced expression of indolamine 2,3-dioxygenase is essential for its protective effects.

Indexed as

AnimalsAntigens, CDCD83 AntigenColitisDextran SulfateDisease Models, AnimalGastrointestinal TractGene ExpressionImmunoglobulinsIndoleamine-Pyrrole 2,3,-DioxygenaseLeukocytesLymph NodesMembrane GlycoproteinsMesenteryMiceAntigens, CDCD83 AntigenDextran SulfateImmunoglobulinsIndoleamine-Pyrrole 2,3,-DioxygenaseMembrane Glycoproteins

Identifiers

PMID24424524
OpenAlexW1979707038

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.