Journal
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 121, Issue 6, Pages 1337-1343Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2008.01.022
Keywords
antimicrobial peptides; atopic dermatitis; barrier function; barrier repair; cytokines; filaggrin; pH; psychologic stress; Staphylococcus aureus; serine proteases; T(H)2 cells
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Funding
- NIAMS NIH HHS [R01 AR019098, AR19098, R01 AR019098-30] Funding Source: Medline
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Until quite recently, the pathogenesis of atopic dermatitis (AD) has been attributed to primary abnormalities of the immune system. Intensive study revealed the key roles played by T(H)1/T(H)2 cell dysregulation, IgE production, mast cell hyperactivity, and dendritic cell signaling in the evolution of the chronic, pruritic, inflammatory dermatosis that characterizes AD. Accordingly, current therapy has been largely directed toward ameliorating T(H)2-mediated inflammation and pruritus. In this review we will assess emerging evidence that inflammation in AD results from inherited and acquired insults to the barrier and the therapeutic implications of this paradigm.
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