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Curr Opin Allergy Clin Immunol. 2009 Oct;9(5):437-46. doi: 10.1097/ACI.0b013e32832e7d36.

Abnormal skin barrier in the etiopathogenesis of atopic dermatitis.

Author information

1
Veterans Affairs Medical Center, Department of Dermatology, University of California, San Francisco, 94121, USA. eliasp@derm.ucsf.edu

Abstract

PURPOSE OF REVIEW:

Many recent studies have revealed the key roles played by Th1/Th2 cell dysregulation, IgE production, mast cell hyperactivity, and dendritic cell signaling in the pathogenesis of atopic dermatitis. Accordingly, current therapy has been largely directed towards ameliorating Th2-mediated inflammation and/or pruritus. We will review here emerging evidence that the inflammation in atopic dermatitis results from inherited and acquired insults to the barrier and the therapeutic implications of this new paradigm.

RECENT FINDINGS:

Recent molecular genetic studies have shown a strong association between mutations in FILAGGRIN and atopic dermatitis, particularly in Northern Europeans. But additional acquired stressors to the barrier are required to initiate inflammation. Sustained hapten access through a defective barrier stimulates a Th1 --> Th2 shift in immunophenotype, which in turn further aggravates the barrier. Secondary Staphylococcus aureus colonization not only amplifies inflammation but also further stresses the barrier in atopic dermatitis.

SUMMARY:

These results suggest a new 'outside-to-inside, back to outside' paradigm for the pathogenesis of atopic dermatitis. This new concept is providing impetus for the development of new categories of 'barrier repair' therapy.

PMID:
19550302
PMCID:
PMC2852024
DOI:
10.1097/ACI.0b013e32832e7d36
[Indexed for MEDLINE]
Free PMC Article
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