Evidence map›Paper›PMID 24715253›Full record

ReviewClinical reviews in allergy & immunology2014

Molecular biology of atopic dermatitis.

Zhanglei Mu, Yan Zhao, Xiaojing Liu, Christopher Chang, Jianzhong Zhang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 92 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Biomedicines · 2025
    Article
  6. Review
  7. Effects of Earthworm (Heliyon · 2025
    Article
  8. Article
  9. Review
  10. Advanced In Vitro Three-Dimensional Skin Models of Atopic Dermatitis.Tissue engineering and regenerative medicine · 2023
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Transcutaneous penetration of a single-chain variable fragment (scFv) compared to a full-size antibody: potential tool for atopic dermatitis (AD) treatment.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2021
    Article
  17. Article
  18. Review
  19. Article
  20. 2,3,7,8-Tetrachlorodibenzo-Annals of dermatology · 2020
    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

5 authors at 3 institutions in 2 countries.

Zhanglei MuDepartment of Dermatology, Peking University People's Hospital, No11, Xizhimen South Street, Beijing, 100044, China.
Yan Zhao
Xiaojing Liu
Christopher Chang
Jianzhong Zhang
Peking University · CNAlfred I. duPont Hospital for Children · USPeking University People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease with specific genetic and immunological mechanisms. The rapid development of new techniques in molecular biology had ushered in new discoveries on the role of cytokines, chemokines, and immune cells in the pathogenesis of AD. New polymorphisms of AD are continually being reported in different populations. The physical and immunological barrier of normal intact skin is an important part of the innate immune system that protects the host against microbials and allergens that are associated with AD. Defects in the filaggrin gene FLG may play a role in facilitating exposure to allergens and microbial pathogens, which may induce Th2 polarization. Meanwhile, Th22 cells also play roles in skin barrier impairment through IL-22, and AD is often considered to be a Th2/Th22-dominant allergic disease. Mast cells and eosinophils are also involved in the inflammation via Th2 cytokines. Release of pruritogenic substances by mast cells induces scratching that further disrupts the skin barrier. Th1 and Th17 cells are mainly involved in chronic phase of AD. Keratinocytes also produce proinflammatory cytokines such as thymic stromal lymphopoietin (TSLP), which can further affect Th cells balance. The immunological characteristics of AD may differ for various endotypes and phenotypes. Due to the heterogeneity of the disease, and the redundancies of these mechanisms, our knowledge of the pathophysiology of the disease is still incomplete, which is reflected by the absence of a cure for the disease.

Indexed as

AllergensChemokinesDermatitis, AtopicEosinophilsFilaggrin ProteinsGene Expression RegulationGenetic HeterogeneityHumansInterleukin-22InterleukinsIntermediate Filament ProteinsKeratinocytesMast CellsSkinTh17 CellsTh1 CellsAllergensChemokinesFilaggrin ProteinsFLG protein, humanInterleukin-22InterleukinsIntermediate Filament Proteins

Identifiers

PMID24715253
OpenAlexW2397939152

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.