Evidence map›Paper›PMID 31749790›Full record

ReviewFrontiers in immunology2019

Genetics and Omics Analysis of Autoimmune Skin Blistering Diseases.

Michael Olbrich, Axel Künstner, Mareike Witte, Hauke Busch, Anke Fähnrich

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  6. Identification of key genes and molecular mechanisms of chronic urticaria based on bioinformatics.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024
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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 1 institution in 1 country.

Michael OlbrichMedical Systems Biology, Institute of Experimental Dermatology, University of Lübeck, Lübeck, Germany.
Axel KünstnerMedical Systems Biology, Institute of Experimental Dermatology, University of Lübeck, Lübeck, Germany.
Mareike WitteDepartment of Dermatology, University of Lübeck, Lübeck, Germany.
Hauke BuschMedical Systems Biology, Institute of Experimental Dermatology, University of Lübeck, Lübeck, Germany.
Anke FähnrichMedical Systems Biology, Institute of Experimental Dermatology, University of Lübeck, Lübeck, Germany.
University of Lübeck · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune blistering diseases (AIBDs) of the skin are characterized by autoantibodies against different intra-/extracellular structures within the epidermis and at the basement membrane zone (BMZ). Binding of the antibodies to their target antigen leads to inflammation at the respective binding site and degradation of these structures, resulting in the separation of the affected skin layers. Clinically, blistering, erythema and lesions of the skin and/or mucous membranes can be observed. Based on the localization of the autoantigen, AIBDs can be divided into pemphigus (intra-epidermal blistering diseases) and pemphigoid diseases (sub-epidermal blistering diseases), respectively. Although autoantigens have been extensively characterized, the underlying causes that trigger the diseases are still poorly understood. Besides the environment, genetic factors seem to play an important role in a predisposition to AIBDs. Here, we review currently known genetic and immunological mechanisms that contribute to the pathogenesis of AIBDs. Among the most commonly encountered genetic predispositions for AIBDs are the HLA gene region, and deleterious mutations of key genes for the immune system. Particularly, HLA class II genes such as the

Indexed as

AutoantigensAutoimmune DiseasesGenetic Predisposition to DiseaseGenomicsSkin Diseases, VesiculobullousAllelesHLA-DQ AntigensHLA-DR AntigensHumansRisk FactorsAutoantigensHLA-DQ AntigensHLA-DR Antigensautoantigensautoimmune bullous diseasesgeneticsHLA class II genessystems medicinetranscriptomics

Identifiers

PMID31749790
PMCPMC6843061
OpenAlexW2980458092

What OpenQuestion holds

Textmetadata
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.