Evidence map›Paper›PMID 28273946›Full record

ArticleScientific reports2017

Dysregulation of mCD46 and sCD46 contribute to the pathogenesis of bullous pemphigoid.

Pei Qiao, Erle Dang, Tianyu Cao, Hui Fang, Jieyu Zhang, Hongjiang Qiao, Gang Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Genome-wide transcriptome analysis identifies novel dysregulated genes implicated in Alzheimer's pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020
    Article
  8. Review
  9. Article
  10. Proteases in Pemphigoid Diseases.Frontiers in immunology · 2019
    Review
  11. Review
  12. Article
  13. 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

7 authors at 2 institutions in 1 country.

Pei QiaoDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Erle DangDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Tianyu CaoDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Hui FangDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Jieyu ZhangDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Hongjiang QiaoDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Gang WangDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China. xjwgang@fmmu.edu.cn.
Air Force Medical University · CNXijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bullous pemphigoid (BP) is an autoimmune bullous disease caused by autoantibodies against BP180 in the epidermal basement membrane. Autoantibody-mediated complement activation is an important process in BP pathogenesis. CD46, a crucial complement regulatory protein in the complement activation, has been reported to be involved in several autoimmune diseases. In the present study, we investigated whether CD46 plays a role in BP development. We found that sCD46 expression was significantly increased in the serum and blister fluids of BP patients and correlated with the levels of anti-BP180 NC16A antibody and C3a. Otherwise, the level of mCD46 was decreased in lesions of BP patients, whereas the complement activation was enhanced. We also found that CD46 knockdown in HaCaT human keratinocytes enhanced autoantibody-mediated complement activation. Importantly, exogenous CD46 blocked complement activation in both healthy skin sections and keratinocytes induced by exposure to pathogenic antibodies from BP patients. These data suggest that CD46 deficiency is an important factor in BP pathogenesis and that increasing CD46 levels might be an effective treatment for BP.

Indexed as

AdultAgedAged, 80 and overAutoantibodiesCase-Control StudiesCell LineComplement ActivationComplement C3aFemaleGene Expression RegulationGene Knockdown TechniquesHumansKeratinocytesMaleMembrane Cofactor ProteinMiddle AgedAutoantibodiesCD46 protein, humanComplement C3aMembrane Cofactor Protein

Identifiers

PMID28273946
PMCPMC5428046
OpenAlexW2594688666

What OpenQuestion holds

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LicenceCC BY
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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.