Evidence map›Paper›PMID 20952584›Full record

ArticleThe American journal of pathology2010

Autoimmunity to desmocollin 3 in pemphigus vulgaris.

Xuming Mao, Arielle R Nagler, Sara A Farber, Eun Jung Choi, Lauren H Jackson, Kristin M Leiferman, Norito Ishii, Takashi Hashimoto, Masayuki Amagai, John J Zone and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. 1-L Transcription of SARS-CoV-2 Spike Protein S1 Subunit.International journal of molecular sciences · 2024
    Article
  4. Article
  5. Review
  6. Review
  7. Dsg3 epitope-specific signalling in pemphigus.Frontiers in immunology · 2023
    Article
  8. In Vitro, Ex Vivo, and In Vivo Models for the Study of Pemphigus.International journal of molecular sciences · 2022
    Review
  9. [Pemphigus vulgaris with exclusive affectation in the esophagus: a case report].Revista medica del Instituto Mexicano del Seguro Social · 2022
    Article
  10. Review
  11. Review
  12. Article
  13. Article
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  15. 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

11 authors at 4 institutions in 2 countries.

Xuming MaoDepartment of Dermatology, University of Pennsylvania, Philadelphia, Pennsylvania, PA, USA.
Arielle R Nagler
Sara A Farber
Eun Jung Choi
Lauren H Jackson
Kristin M Leiferman
Norito Ishii
Takashi Hashimoto
Masayuki Amagai
John J Zone
Aimee S Payne
University of Pennsylvania · USUniversity of Utah · USKurume University · JPKeio University · JP

Funding

Understanding molecular mechanisms underlying the formation of the blue nevus andP30AR057217 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI COTSARELIS, GEORGE · 2009 to 2013
$3.2M
Role of autoantibody isotype in pemphigus pathogenesisR01AR057001 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI PAYNE, AIMEE S · 2010 to 2014
$1.7M
Cloning and characterization of human pemphigus autoantibodiesK08AR053505 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI PAYNE, AIMEE S · 2007 to 2011
$638k
NIAMS NIH HHS K08 AR053505NIAMS NIH HHS K08-AR053505NIAMS NIH HHS P30 AR057217NIAMS NIH HHS P30-AR057217NIAMS NIH HHS R01 AR057001
6 · The paper itself

Abstract

Pemphigus vulgaris is a blistering disease associated with autoantibodies to the desmosomal adhesion protein, desmoglein 3. Genetic deficiency of desmoglein 3 in mice mimics autoimmunity to desmoglein 3 in pemphigus vulgaris, with mucosal-dominant blistering in the suprabasal layer of the epidermis. Mice with an epidermal-specific deletion of desmocollin 3, the other major desmosomal cadherin isoform expressed in the basal epidermis, develop suprabasal blisters in skin that are histologically identical to those observed in pemphigus vulgaris, suggesting that desmocollin 3 might be a target of autoantibodies in some pemphigus vulgaris patients. We now demonstrate that desmocollin 3 is an autoantigen in pemphigus vulgaris, illustrated in a patient with mucosal-dominant blistering. Six of 38 pemphigus vulgaris and one of 85 normal serum samples immunoprecipitate desmocollin 3 (P = 0.003). Incubation of patient IgG with human keratinocytes causes loss of intercellular adhesion, and adsorption with recombinant desmocollin 3 specifically prevents this pathogenic effect. Additionally, anti-desmocollin 3 sera cause loss of keratinocyte cell surface desmocollin 3, but not desmoglein 3 by immunofluorescence, indicating distinct cellular pathogenic effects in anti-desmocollin and anti-desmoglein pemphigus, despite their identical clinical presentations. These data demonstrate that desmocollin 3 is a pathogenic autoantigen in pemphigus vulgaris and suggest that pemphigus vulgaris is a histological reaction pattern that may result from autoimmunity to desmoglein 3, desmocollin 3, or both desmosomal cadherins.

Indexed as

AnimalsAutoantibodiesAutoimmunityCase-Control StudiesCell MembraneCells, CulturedDesmocollinsDesmoglein 3FemaleHumansInfant, NewbornKeratinocytesMiddle AgedPemphigusProtein Processing, Post-TranslationalSeroepidemiologic StudiesAutoantibodiesDesmocollinsDesmoglein 3DSC3 protein, humanDSG3 protein, human

Identifiers

PMID20952584
PMCPMC2993297
OpenAlexW2098492858

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.