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Related Experiment Video

Updated: Jun 20, 2026

Resolving Water, Proteins, and Lipids from In Vivo Confocal Raman Spectra of Stratum Corneum through a Chemometric Approach
09:32

Resolving Water, Proteins, and Lipids from In Vivo Confocal Raman Spectra of Stratum Corneum through a Chemometric Approach

Published on: September 26, 2019

Filaggrin in atopic dermatitis.

Grainne M O'Regan1, Aileen Sandilands, W H Irwin McLean

  • 1Department of Paediatric Dermatology, Our Lady's Children's Hospital, Dublin, Ireland.

The Journal of Allergy and Clinical Immunology
|September 2, 2009
PubMed
Summary
This summary is machine-generated.

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Loss-of-function mutations in the filaggrin gene (FLG) are a major risk factor for eczema. This highlights the role of epithelial barrier defects in eczema pathogenesis, alongside immune responses.

Area of Science:

  • Dermatology
  • Genetics
  • Immunology

Background:

  • Eczema pathogenesis was historically viewed as primarily immunologic.
  • Recent genetic studies identify filaggrin (FLG) mutations as a significant risk factor for eczema.
  • This challenges previous understandings and suggests a role for epithelial barrier dysfunction.

Purpose of the Study:

  • To review recent advances in understanding the genetics of filaggrin (FLG) in eczema.
  • To explore the role of FLG mutations in the pathogenesis of eczema and related atopic disorders.
  • To synthesize current knowledge on the transition from inherited barrier defects to clinical eczema.

Main Methods:

  • Review of recent genetic studies on filaggrin (FLG) mutations.
  • Analysis of proposed unifying hypotheses for eczema pathogenesis.

Related Experiment Videos

Last Updated: Jun 20, 2026

Resolving Water, Proteins, and Lipids from In Vivo Confocal Raman Spectra of Stratum Corneum through a Chemometric Approach
09:32

Resolving Water, Proteins, and Lipids from In Vivo Confocal Raman Spectra of Stratum Corneum through a Chemometric Approach

Published on: September 26, 2019

  • Synthesis of evidence linking barrier defects to inflammatory responses.

    • Main Results:

    • Loss-of-function mutations in the filaggrin gene (FLG) are a major risk factor for eczema.
    • FLG mutations support a unifying hypothesis involving epithelial barrier defects and immune responses.
    • Perturbed barrier function is implicated in eczema pathogenesis for many patients.

    Conclusions:

    • Filaggrin gene (FLG) genetics provides crucial insights into eczema development.
    • A heritable epithelial barrier defect is a key factor in eczema pathogenesis.
    • Further research is needed to understand FLG's role in atopic disorders and modifying factors.