Evidence map›Paper›PMID 26385242›Full record

ReviewClinical reviews in allergy & immunology2016

The Genetics and Epigenetics of Atopic Dermatitis-Filaggrin and Other Polymorphisms.

Yunsheng Liang, Christopher Chang, Qianjin Lu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 5 pooled it
11.0field-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

75 citing papers in PubMed, 5 syntheses or guidelines pooled it, 164 citations in OpenAlex.

  1. Gene variants associated with skin barrier dysfunction in atopic dermatitis: a systematic review and meta-analysis.Revista paulista de pediatria : orgao oficial da Sociedade de Pediatria de Sao Paulo · 2025
    Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Trial
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

15 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 2 countries.

Yunsheng LiangHunan Key Laboratory of Medical Epigenomics & Department of Dermatology, The Second Xiangya Hospital, Central South University, 139 Renmin Middle Rd, Changsha, Hunan, 410011, China.
Christopher ChangDivision of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, Davis, CA, 95616, USA.
Qianjin LuHunan Key Laboratory of Medical Epigenomics & Department of Dermatology, The Second Xiangya Hospital, Central South University, 139 Renmin Middle Rd, Changsha, Hunan, 410011, China. epigenetics2010@126.com.
Central South University · CNSecond Xiangya Hospital of Central South University · CNUniversity of California, Davis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease caused by a combination of genetic and environmental factors. Genetic evidences depict a complex network comprising by epidermal barrier dysfunctions and dysregulation of innate and adaptive immunity in the pathogenesis of AD. Mutations in the human filaggrin gene (FLG) are the most significant and well-replicated genetic mutation associated with AD, and other mutations associated with epidermal barriers such as SPINK5, FLG-2, SPRR3, and CLDN1 have all been linked to AD. Gene variants may also contribute to the abnormal innate and adaptive responses found in AD, including mutations in PRRs and AMPs, TSLP and TSLPR, IL-1 family cytokines and receptors genes, vitamin D pathway genes, FCER1A, and Th2 and other cytokines genes. GWAS and Immunochip analysis have identified a total of 19 susceptibility loci for AD. Candidate genes at these susceptibility loci identified by GWAS and Immunochip analysis also suggest roles for epidermal barrier functions, innate and adaptive immunity, interleukin-1 family signaling, regulatory T cells, the vitamin D pathway, and the nerve growth factor pathway in the pathogenesis of AD. Increasing evidences show the modern lifestyle (i.e., the hygiene hypothesis, Western diet) and other environmental factors such as pollution and environmental tobacco smoke (ETS) lead to the increasing prevalence of AD with the development of industrialization. Epigenetic alterations in response to these environmental factors, including DNA methylation and microRNA related to immune system and skin barriers, have been found to contribute to the pathogenesis of AD. Genetic variants and epigenetic alteration might be the key tools for the molecular taxonomy of AD and provide the background for the personalized management.

Indexed as

Epigenesis, GeneticGenetic Association StudiesGenetic Predisposition to DiseasePolymorphism, GeneticAnimalsCytokinesDermatitis, AtopicEnvironmentEpidermisFilaggrin ProteinsGene-Environment InteractionGenome-Wide Association StudyHumansImmune SystemIntermediate Filament ProteinsMutationCytokinesFilaggrin ProteinsFLG2 protein, humanFLG protein, humanIntermediate Filament ProteinsReceptors, CytokineAtopic dermatitisEpidermal barrierEpigeneticsFilaggrinGeneticsPolymorphism

Identifiers

PMID26385242
OpenAlexW1716968389

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.