Evidence map›Paper›PMID 9710446›Full record

ArticleThe Journal of clinical investigation1998

Antibodies against desmoglein 3 (pemphigus vulgaris antigen) are present in sera from patients with paraneoplastic pemphigus and cause acantholysis in vivo in neonatal mice.

M Amagai, T Nishikawa, H C Nousari, G J Anhalt, T Hashimoto

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
16.7field-weighted citation impact, top 1% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 315 citations in OpenAlex.

  1. Guideline
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  6. JAK inhibition decreases the autoimmune burden in Down syndrome.medRxiv : the preprint server for health sciences · 2024
    Article
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  11. A gene-centric approach to biomarker discovery identifies transglutaminase 1 as an epidermal autoantigen.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  12. Autoimmune Pemphigus: Latest Advances and Emerging Therapies.Frontiers in molecular biosciences · 2021
    Review
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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

5 authors at 3 institutions in 2 countries.

M AmagaiDepartment of Dermatology, Keio University School of Medicine, Tokyo 160-8582, Japan. amagai@mc.med.keio.ac.jp
T Nishikawa
H C Nousari
G J Anhalt
T Hashimoto
Johns Hopkins University · USKeio University · JPKurume University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Paraneoplastic pemphigus (PNP) is an autoimmune blistering disease that occurs in association with underlying neoplasms. Patients with PNP develop characteristic IgG autoantibodies directed against multiple antigens, most of which have been identified as cytoplasmic proteins of the plakin family (desmoplakin I, II, BPAG1, envoplakin, and periplakin). This study identified cell surface target antigens of PNP. We focused on desmoglein (Dsg) 3 and Dsg1, the autoantigens of pemphigus vulgaris and pemphigus foliaceus. ELISA using baculovirus-expressed recombinant Dsgs (rDsg3, rDsg1) has revealed that 25 out of 25 PNP sera tested were positive against Dsg3 and 16 of 25 were positive against Dsg1. All of 12 PNP sera tested immunoprecipitated Dsg3. Removal of anti-Dsg3 autoantibodies by immunoadsorption was sufficient to eliminate the ability of PNP sera to induce cutaneous blisters in neonatal mice in vivo. Furthermore, anti-Dsg3-specific antibodies that were affinity purified from PNP sera were proven to be pathogenic and caused blisters in neonatal mice. These findings indicate that Dsg3 and Dsg1 are the cell surface target antigens in PNP and that IgG autoantibodies against Dsg3 in PNP sera play a pathogenic role in inducing loss of cell adhesion of keratinocytes and causing blister formation.

Indexed as

AcantholysisAnimalsAnimals, NewbornAutoantibodiesAutoantigensBlisterCadherinsDesmoglein 1Desmoglein 3HumansMiceParaneoplastic SyndromesPemphigusSkinAutoantibodiesAutoantigensCadherinsDesmoglein 1Desmoglein 3DSG3 protein, human

Identifiers

PMID9710446
PMCPMC508940
OpenAlexW2009741791

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.