Evidence map›Paper›PMID 15841169›Full record

ArticleThe Journal of clinical investigation2005

The pathophysiology of autoimmune blistering diseases.

Kim B Yancey

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Article
  3. Coagulation and Skin Autoimmunity.Frontiers in immunology · 2019
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Mechanisms mediating the vesicant actions of sulfur mustard after cutaneous exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2010
    Review
  13. Article
  14. Article
  15. Radio-induced bullous pemphigoid.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2010
    Article
  16. Coagulation activation in autoimmune bullous diseases.Clinical and experimental immunology · 2009
    Article
  17. Article
  18. Article
  19. The desmosome and pemphigus.Histochemistry and cell biology · 2008
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Kim B YanceyDepartment of Dermatology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226-4801, USA. kyancey@mcw.edu
Medical College of Wisconsin · US

Funding

A Transgenic Animal Model for PemphigoidR01AR048982 · NIAMS · UT SOUTHWESTERN MEDICAL CENTER · PI YANCEY, KIM BRUCE · 2003 to 2007
$1.4M
NIAMS NIH HHS R01 AR048982NIAMS NIH HHS R01 AR048982-01A1
6 · The paper itself

Abstract

Knowledge of the pathophysiology of immunobullous diseases has been advanced by the demonstration that passive transfer of antibodies against skin autoantigens can induce blisters in experimental animals with clinical, histologic, and immunopathologic features similar to those seen in human patients. In this issue of the JCI, Liu et al. extend their earlier observations regarding an experimental murine model of bullous pemphigoid by showing that the plasminogen/plasmin signaling cascade synergizes with MMP-9 during the early phase of antibody-induced blister formation in vivo. In a separate study, Sitaru et al. show for the first time to my knowledge that passive transfer of experimental antibodies against type VII collagen create subepidermal blisters in mice that mimic those seen in patients with epidermolysis bullosa acquisita (see the related article beginning on page 870). While the articles by Liu, Sitaru, and their colleagues identify pathways of inflammation and tissue injury that, if interrupted, may abrogate blister formation, in a third study, Payne et al. utilized phage display technologies to isolate human anti-desmoglein monoclonal antibodies from a patient with pemphigus vulgaris and show that such antibodies have restricted patterns of heavy and light chain gene usage - findings suggesting that autoantibodies may represent an additional target for therapeutic interventions in patients with immunobullous diseases (see the related article beginning on page 888).

Indexed as

AnimalsAutoantigensAutoimmune DiseasesBasement MembraneCollagen Type XVIIDisease Models, AnimalHumansImmunization, PassiveImmunoglobulin GMatrix Metalloproteinase 9MiceNon-Fibrillar CollagensSignal TransductionSkin Diseases, VesiculobullousAutoantigensCollagen Type XVIIImmunoglobulin GMatrix Metalloproteinase 9Non-Fibrillar Collagens

Identifiers

PMID15841169
PMCPMC1070439
OpenAlexW2112890758

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.