Journal
CURRENT OPINION IN ALLERGY AND CLINICAL IMMUNOLOGY
Volume 9, Issue 5, Pages 437-446Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/ACI.0b013e32832e7d36
Keywords
antimicrobial peptides; atopic dermatitis; barrier function; barrier repair
Categories
Funding
- National Institutes of Health (NIH) [AR019098]
- Department of Defense (DOD) [W81XWH-05-2-0094]
- Medical Research Service, Department of Veterans Affairs
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR019098] Funding Source: NIH RePORTER
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available