Evidence map›Paper›PMID 26597100›Full record

ReviewSeminars in immunopathology2016

Immune response in pemphigus and beyond: progresses and emerging concepts.

Giovanni Di Zenzo, Kyle T Amber, Beyza S Sayar, Eliane J Müller, Luca Borradori

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Seminars in immunopathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03177213 (Serum IL-21 Levels in Patients With Pemphigus Vulgaris), which is not on this map. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
5.1field-weighted citation impact, top 4% 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.

NCT03177213 unknown statusnot on this mapstarted 2017, after this paper: background citation

Serum IL-21 Levels in Patients With Pemphigus Vulgaris

TypeobservationalSponsorAssiut UniversityRan2017 to 2018Enrolled20ConditionsPemphigus Vulgaris
3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Dsg3 epitope-specific signalling in pemphigus.Frontiers in immunology · 2023
    Article
  14. Review
  15. Article
  16. Article
  17. The Immunogenetics of Autoimmune Blistering Diseases.Advances in experimental medicine and biology · 2022
    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

5 authors at 3 institutions in 3 countries.

Giovanni Di ZenzoLaboratory of Molecular and Cell Biology, Istituto Dermopatico dell'Immacolata, IDI-IRCCS, Rome, Italy.
Kyle T AmberDepartment of Dermatology, University of California Irvine Health, Irvine, CA, USA.
Beyza S SayarVetsuisse Faculty, Molecular Dermatology and Stem Cell Research, Institute of Animal Pathology, Bern, Switzerland.
Eliane J MüllerVetsuisse Faculty, Molecular Dermatology and Stem Cell Research, Institute of Animal Pathology, Bern, Switzerland. Eliane.Mueller@vetsuisse.unibe.ch.
Luca BorradoriVetsuisse Faculty, DermFocus, Bern, Switzerland. Luca.Borradori@insel.ch.
Istituto Dermopatico dell'Immacolata · ITUniversity Hospital of Bern · CHUniversity of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pemphigus vulgaris (PV) and pemphigus foliaceus (PF) are two severe autoimmune bullous diseases of the mucosae and/or skin associated with autoantibodies directed against desmoglein (Dsg) 3 and/or Dsg1. These two desmosomal cadherins, typifying stratified epithelia, are components of cell adhesion complexes called desmosomes and represent extra-desmosomal adhesion receptors. We herein review the advances in our understanding of the immune response underlying pemphigus, including human leucocyte antigen (HLA) class II-associated genetic susceptibility, characteristics of pathogenic anti-Dsg antibodies, antigenic mapping studies as well as findings about Dsg-specific B and T cells. The pathogenicity of anti-Dsg autoantibodies has been convincingly demonstrated. Disease activity and clinical phenotype correlate with anti-Dsg antibody titers and profile while passive transfer of anti-Dsg IgG from pemphigus patients' results in pemphigus-like lesions in neonatal and adult mice. Finally, adoptive transfer of splenocytes from Dsg3-knockout mice immunized with murine Dsg3 into immunodeficient mice phenotypically recapitulates PV. Although the exact pathogenic mechanisms leading to blister formation have not been fully elucidated, intracellular signaling following antibody binding has been found to be necessary for inducing cell-cell dissociation, at least for PV. These new insights not only highlight the key role of Dsgs in maintenance of tissue homeostasis but are expected to progressively change pemphigus management, paving the way for novel targeted immunologic and pharmacologic therapies.

Indexed as

AnimalsAntibodies, MonoclonalAutoantibodiesAutoantigensDesmogleinsDisease ProgressionEpitopesGenetic Predisposition to DiseaseHumansImmune SeraImmunoglobulin IdiotypesMutationOrgan SpecificityPemphigusSignal TransductionT-Lymphocyte SubsetsAntibodies, MonoclonalAutoantibodiesAutoantigensDesmogleinsEpitopesImmune SeraImmunoglobulin IdiotypesAcantholysisAutoantibodyCadherinsCell-cell adhesionDesmogleinDesmosomeFogo selvagemMature desmogleinMonoclonal antibodyPathogenesisPemphigus foliaceusPemphigus vulgarisPrecursor DsgSignaling pathways

Identifiers

PMID26597100
OpenAlexW2342974512

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.