Evidence map›Paper›PMID 31732776›Full record

ReviewSeminars in immunopathology2019

Resolution in bullous pemphigoid.

Christian D Sadik, Enno Schmidt

Open access · hybridAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.5field-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

14 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Research in practice: Immune checkpoint inhibitor related autoimmune bullous dermatosis.Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Dyshidrosiform Bullous Pemphigoid.Medicina (Kaunas, Lithuania) · 2021
    Review
  12. Article
  13. Article
  14. 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

2 authors at 2 institutions in 1 country.

Christian D SadikDepartment of Dermatology, Allergy, and Venerology, University of Lübeck, Lübeck, Germany.
Enno SchmidtDepartment of Dermatology, Allergy, and Venerology, University of Lübeck, Lübeck, Germany. enno.schmidt@uksh.de.ORCID 0000-0002-1206-8913
Universitäres Kinderwunschzentrum Lübeck · DEUniversity of Lübeck · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pemphigoid diseases are a group of autoimmune blistering skin diseases defined by an immune response against certain components of the dermal-epidermal adhesion complex. They are prototypical, autoantibody-driven, organ-specific diseases with the emergence of inflammatory skin lesions dependent on the recruitment of immune cells, particularly granulocytes, into the skin. During an acute flare of disease, inflammatory skin lesions typically progressing from erythema through urticarial plaques to subepidermal blisters erosions erupt and, finally, completely resolve, thus illustrating that resolution of inflammation is continuously executed in pemphigoid disease patients and can be directly monitored on the skin. Despite these superb conditions for examining resolution in pemphigoid diseases as paradigm diseases for antibody-induced tissue inflammation, the mechanisms of resolution in pemphigoid are underinvestigated and still largely elusive. In the last decade, mouse models for pemphigoid diseases were developed, which have been instrumental to identify several key pathways for the initiation of inflammation in these diseases. More recently, also protective pathways, specifically IL-10 and C5aR2 signalling on the molecular level and T

Indexed as

AnimalsAutoimmunityBiomarkersDisease ManagementDisease SusceptibilityEpidermisHumansInflammation MediatorsLipid MetabolismPemphigoid, BullousSkinBiomarkersInflammation MediatorsAutoimmunityBlisteringBullous pemphigoidComplementIL-17PathophysiologyResolution

Identifiers

PMID31732776
PMCPMC6881416
OpenAlexW2986159963

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.