Evidence map›Paper›PMID 23505434›Full record

ArticlePloS one2013

Pemphigus vulgaris autoantibody profiling by proteomic technique.

Mina Kalantari-Dehaghi, Grant J Anhalt, Michael J Camilleri, Alex I Chernyavsky, Sookhee Chun, Philip L Felgner, Algis Jasinskas, Kristin M Leiferman, Li Liang, Steve Marchenko and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 3% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Observational
  5. Article
  6. Review
  7. Dsg3 epitope-specific signalling in pemphigus.Frontiers in immunology · 2023
    Article
  8. Article
  9. Article
  10. Apoptolysis: a less understood concept in the pathogenesis of Pemphigus Vulgaris.Apoptosis : an international journal on programmed cell death · 2022
    Review
  11. Review
  12. Autoimmune Pemphigus: Latest Advances and Emerging Therapies.Frontiers in molecular biosciences · 2021
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

14 authors at 4 institutions in 1 country.

Mina Kalantari-DehaghiDepartment of Dermatology, University of California Irvine, Irvine, California, United States of America. mkalanta@uci.edu
Grant J Anhalt
Michael J Camilleri
Alex I Chernyavsky
Sookhee Chun
Philip L Felgner
Algis Jasinskas
Kristin M Leiferman
Li Liang
Steve Marchenko
Rie Nakajima-Sasaki
Mark R Pittelkow
John J Zone
Sergei A Grando
University of California, Irvine · USMayo Clinic · USUniversity of Utah · USJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pemphigus vulgaris (PV) is a mucocutaneous blistering disease characterized by IgG autoantibodies against the stratified squamous epithelium. Current understanding of PV pathophysiology does not explain the mechanism of acantholysis in patients lacking desmoglein antibodies, which justifies a search for novel targets of pemphigus autoimmunity. We tested 264 pemphigus and 138 normal control sera on the multiplexed protein array platform containing 701 human genes encompassing many known keratinocyte cell-surface molecules and members of protein families targeted by organ-non-specific PV antibodies. The top 10 antigens recognized by the majority of test patients' sera were proteins encoded by the DSC1, DSC3, ATP2C1, PKP3, CHRM3, COL21A1, ANXA8L1, CD88 and CHRNE genes. The most common combinations of target antigens included at least one of the adhesion molecules DSC1, DSC3 or PKP3 and/or the acetylcholine receptor CHRM3 or CHRNE with or without the MHC class II antigen DRA. To identify the PV antibodies most specific to the disease process, we sorted the data based on the ratio of patient to control frequencies of antigen recognition. The frequency of antigen recognition by patients that exceeded that of control by 10 and more times were the molecules encoded by the CD33, GP1BA, CHRND, SLC36A4, CD1B, CD32, CDH8, CDH9, PMP22 and HLA-E genes as well as mitochondrial proteins encoded by the NDUFS1, CYB5B, SOD2, PDHA1 and FH genes. The highest specificity to PV showed combinations of autoantibodies to the calcium pump encoded by ATP2C1 with C5a receptor plus DSC1 or DSC3 or HLA-DRA. The results identified new targets of pemphigus autoimmunity. Novel autoantibody signatures may help explain individual variations in disease severity and treatment response, and serve as sensitive and specific biomarkers for new diagnostic assays in PV patients.

Indexed as

ProteomicsAntibody SpecificityAutoantibodiesAutoantigensDesmoglein 3HumansPemphigusPrincipal Component AnalysisProtein Array AnalysisSensitivity and SpecificityAutoantibodiesAutoantigensDesmoglein 3DSG3 protein, human

Identifiers

PMID23505434
PMCPMC3591405
OpenAlexW2073775962

What OpenQuestion holds

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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.