Evidence map›Paper›PMID 18055547›Full record

ArticleThe American journal of pathology2007

Indoleamine 2,3-dioxygenase (IDO): the antagonist of type I interferon-driven skin inflammation?

Marina Scheler, Joerg Wenzel, Thomas Tüting, Osamu Takikawa, Thomas Bieber, Dagmar von Bubnoff

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

22 citing papers in PubMed, 58 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Lichen Planus.Frontiers in medicine · 2021
    Review
  6. International journal of molecular sciences · 2020
    Article
  7. Article
  8. The T-win® technology: immune-modulating vaccines.Seminars in immunopathology · 2019
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Self-reactive T cells: suppressing the suppressors.Cancer immunology, immunotherapy : CII · 2014
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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

6 authors at 2 institutions in 2 countries.

Marina SchelerDepartment of Dermatology, Friedrich-Wilhelms University, Sigmund Freud-Strasse 25, 53105 Bonn, Germany. marina.scheler@ukb.uni-bonn.de
Joerg Wenzel
Thomas Tüting
Osamu Takikawa
Thomas Bieber
Dagmar von Bubnoff
University of Bonn · DENational Center for Geriatrics and Gerontology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have provided evidence that a type I interferon (IFN)-driven immune response might play an important role in the pathogenesis of lichen planus (LP), an inflammatory disorder of the skin of unclear etiology. Plasmacytoid dendritic cells in affected skin from LP have been proposed to produce IFN-alpha/beta locally, which leads to the expression of IFN-inducible chemokines such as IP10/CXCL10 in the epidermis. This chemokine recruits chemokine receptor CXCR3-expressing T-lymphocytes into the skin via CXCR3/IP10 interactions. Indoleamine 2,3-dioxygenase (IDO), which degrades tryptophan and suppresses T-cell proliferation, is induced by IFNs and other inflammatory cytokines. We show that type I IFN-mediated skin disorders, such as LP, strongly express IDO in lesional skin. This expression closely correlates to the expression of the highly specific type I IFN marker MxA. We further demonstrate that the IDO+ cells in LP are large myeloid CD11c+S100+CD68(-) dendritic cells. Accordingly, CD11c+ antigen-presenting cells significantly up-regulate IDO gene expression and intracellular IDO protein expression after stimulation with IFN-alpha in vitro. These findings reveal that both proinflammatory and counterregulatory mechanisms are operative in cutaneous lesions of LP. We propose that the balance of these mechanisms may be involved in the pathogenesis of this disorder.

Indexed as

Antigens, CDAntigens, Differentiation, MyelomonocyticCD11c AntigenCD68 MoleculeDendritic CellsDermatitisFemaleHumansIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-alphaInterferon-gammaInterferon Type ILichen PlanusMaleMyeloid CellsPsoriasisAntigens, CDAntigens, Differentiation, MyelomonocyticCD11c AntigenCD68 antigen, humanCD68 MoleculeIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-alphaInterferon-gammaInterferon Type IS100 Proteins

Identifiers

PMID18055547
PMCPMC2111116
OpenAlexW2149791488

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.