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Filaggrin in atopic dermatitis.

Grainne M O'Regan¹, Aileen Sandilands², W H Irwin McLean²

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

The Journal of Allergy and Clinical Immunology

|September 9, 2008

Summary

Mutations in the filaggrin gene (FLG) are a major risk factor for eczema, indicating a heritable epithelial barrier defect contributes to disease pathogenesis. This challenges previous views, suggesting a unifying hypothesis for eczema and related atopic disorders.

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Area of Science:

Dermatology
Genetics
Immunology

Background:

Eczema pathogenesis was historically viewed as primarily immunologic.
Recent discoveries link filaggrin gene (FLG) loss-of-function mutations to eczema risk.
This suggests a significant role for epithelial barrier defects.

Purpose of the Study:

To review recent advances in understanding FLG genetics in eczema.
To explore the link between barrier defects and eczema pathogenesis.
To discuss the role of FLG in atopic disorders.

Main Methods:

Review of genetic studies on filaggrin gene (FLG) mutations.
Synthesis of current hypotheses on eczema pathogenesis.
Analysis of the transition from barrier defect to clinical eczema.

Main Results:

Loss-of-function FLG mutations are a major, replicated risk factor for eczema.
These findings support a unifying hypothesis integrating barrier defects and immune responses.
Perturbed barrier function is implicated in eczema pathogenesis for many patients.

Conclusions:

FLG genetics provides crucial insights into eczema etiology.
Further research is needed on factors modifying FLG expression and other barrier proteins.
Understanding FLG's role is key to unraveling eczema and related atopic diseases.