Evidence map›Paper›PMID 17879094›Full record

ReviewArchives of dermatological research2007

Experimental models for the autoimmune and inflammatory blistering disease, Bullous pemphigoid.

Lisa Leighty, Ning Li, Luis A Diaz, Zhi Liu

Open access · hybridAbstract readReview
In one paragraph

Review in Archives of dermatological research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Observational
  6. Article
  7. Observational
  8. Article
  9. Review
  10. Article
  11. Regulation of mast cell responses in health and disease.Critical reviews in immunology · 2011
    Review
  12. Our perception of the mast cell from Paul Ehrlich to now.European journal of immunology · 2009
    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

4 authors at 1 institution in 1 country.

Lisa LeightyDepartment of Dermatology, University of North Carolina School of Medicine, 3100 Thurston Bowles, Chapel Hill, NC 27599, USA.
Ning Li
Luis A Diaz
Zhi Liu
University of North Carolina at Chapel Hill · US

Funding

ETIOLOGY AND PATHOGENESIS OF PEMPHIGUSR01AR032599 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DIAZ, LUIS A. · 1987 to 2017
$5.2M
IMMUNOPATHOGENESIS OF BULLOUS PEMPHIGOIDR01AI040768 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LIU, ZHI · 2001 to 2016
$4.1M
PEMPHIGUS AND PEMPHIGOIDR01AR032081 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DIAZ, LUIS A. · 1986 to 2011
$3.3M
The Mechanism of IVIG Action in PemphigusR01AI061430 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LIU, ZHI · 2004 to 2006
$999k
Role of Glycosylation of Dsg1 in Pemphigus acantholysisK01AR052109 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LI, NING · 2005 to 2009
$606k
TRAINING GRANT IN DERMATOLOGIC RESEARCHT32AR007369 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DIAZ, LUIS A. · 1986 to 2006
$545k
Role of Apoptosis in PemphigusR03AR053313 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LI, NING · 2006 to 2008
$152k
IMMUNOPATHOGENESIS OF BULLOUS PEMPHIGOIDR29AI040768 · NIAID · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI LIU, ZHI · 1996 to 2000
$101k
PEMPHIGUS AND PEMPHIGOIDR37AR032081 · NIAMS · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI DIAZ, LUIS A. · 1990 to 1999
–
NIAID NIH HHS AI40768NIAID NIH HHS AI61430NIAID NIH HHS R01 AI040768NIAID NIH HHS R01 AI061430NIAID NIH HHS R29 AI040768NIAMS NIH HHS AR053313NIAMS NIH HHS AR32081NIAMS NIH HHS AR32599NIAMS NIH HHS K01 AR052109NIAMS NIH HHS R01 AR032081NIAMS NIH HHS R01 AR032599NIAMS NIH HHS R03 AR053313NIAMS NIH HHS R37 AR032081NIAMS NIH HHS T32 AR007369NIAMS NIH HHS T32 AR07369
6 · The paper itself

Abstract

Bullous pemphigoid (BP) is a subepidermal skin blistering disease characterized immunohistologically by dermal-epidermal junction (DEJ) separation, an inflammatory cell infiltrate in the upper dermis, and autoantibodies targeted toward the hemidesmosomal proteins BP230 and BP180. Development of an IgG passive transfer mouse model of BP that reproduces these key features of human BP has demonstrated that subepidermal blistering is initiated by anti-BP180 antibodies and mediated by complement activation, mast cell degranulation, neutrophil infiltration, and proteinase secretion. This model is not compatible with study of human pathogenic antibodies, as the human and murine antigenic epitopes are not cross-reactive. The development of two novel humanized mouse models for the first time has enabled study of disease mechanisms caused by BP autoantibodies, and presents an ideal in vivo system to test novel therapeutic strategies for disease management.

Indexed as

Disease Models, AnimalPemphigoid, BullousAnimalsAutoantibodiesAutoantigensCollagen Type XVIICricetinaeEpitope MappingGenotypeHumansImmunoglobulin GMiceMice, TransgenicNon-Fibrillar CollagensPhenotypeRabbitsAutoantibodiesAutoantigensCollagen Type XVIIImmunoglobulin GNon-Fibrillar Collagens

Identifiers

PMID17879094
PMCPMC2064945
OpenAlexW1968583141

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.