Evidence map›Paper›PMID 25131691›Full record

ReviewThe Journal of allergy and clinical immunology2014

Mechanisms of abnormal lamellar body secretion and the dysfunctional skin barrier in patients with atopic dermatitis.

Peter M Elias, Joan S Wakefield

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of allergy and clinical immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
19.5field-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

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 231 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. HomologousMaterials today. Bio · 2026
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Skin lamellar bodies: a unique set of lysosome-related organelles.Frontiers in cell and developmental biology · 2025
    Article

36 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

2 authors at 2 institutions in 1 country.

Peter M EliasDermatology Service, Veterans Affairs Medical Center, and the Department of Dermatology, University of California, San Francisco, Calif. Electronic address: eliasp@derm.ucsf.edu.
Joan S WakefieldDermatology Service, Veterans Affairs Medical Center, and the Department of Dermatology, University of California, San Francisco, Calif.
San Francisco VA Medical Center · USUniversity of California, San Francisco · US

Funding

NATURE OF THE MAMMALIAN CUTANEOUS PERMEABILITY BARRIERR01AR019098 · NIAMS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI ELIAS, PETER M · 1986 to 2012
$4.2M
Pathogenesis and Therapy of Ichthyosis in Disorders of Lipid MetabolismR01AR061106 · NIAMS · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI MAURO, THEODORA M · 2012 to 2022
$3.3M
NIAMS NIH HHS AR019098NIAMS NIH HHS R01 AR019098NIAMS NIH HHS R01 AR061106
6 · The paper itself

Abstract

I review how diverse inherited and acquired abnormalities in epidermal structural and enzymatic proteins converge to produce defective permeability barrier function and antimicrobial defense in patients with atopic dermatitis (AD). Although best known are mutations in filaggrin (FLG), mutations in other member of the fused S-100 family of proteins (ie, hornerin [hrn] and filaggrin 2 [flg-2]); the cornified envelope precursor (ie, SPRR3); mattrin, which is encoded by TMEM79 and regulates the assembly of lamellar bodies; SPINK5, which encodes the serine protease inhibitor lymphoepithelial Kazal-type trypsin inhibitor type 1; and the fatty acid transporter fatty acid transport protein 4 have all been linked to AD. Yet these abnormalities often only predispose to AD; additional acquired stressors that further compromise barrier function, such as psychological stress, low ambient humidity, or high-pH surfactants, often are required to trigger disease. T(H)2 cytokines can also compromise barrier function by downregulating expression of multiple epidermal structural proteins, lipid synthetic enzymes, and antimicrobial peptides. All of these inherited and acquired abnormalities converge on the lamellar body secretory system, producing abnormalities in lipid composition, secretion, and/or extracellular lamellar membrane organization, as well as antimicrobial defense. Finally, I briefly review therapeutic options that address this new pathogenic paradigm.

Indexed as

AnimalsBodily SecretionsDermatitis, AtopicFatty Acid Transport ProteinsFilaggrin ProteinsGene-Environment InteractionHumansImmunity, InnateInclusion BodiesIntermediate Filament ProteinsLipid MetabolismMembrane ProteinsProteinase Inhibitory Proteins, SecretoryProteolysisSerine Peptidase Inhibitor Kazal-Type 5SkinFatty Acid Transport ProteinsFilaggrin ProteinsFLG2 protein, humanFLG protein, humanIntermediate Filament ProteinsMembrane ProteinsProteinase Inhibitory Proteins, SecretorySerine Peptidase Inhibitor Kazal-Type 5SPINK5 protein, humanTmem79 protein, humanAntimicrobial peptidesatopic dermatitisbarrier functionceramidescytokinesfilaggrinkallikreinslamellar bodieslipid compositionpHserine protease inhibitorsT(H)2 cells

Identifiers

PMID25131691
PMCPMC4186911
OpenAlexW2041515888

What OpenQuestion holds

Textmetadata
LicenceTDM
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.