Journal
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 134, Issue 4, Pages 769-779Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2014.08.008
Keywords
Atopic dermatitis; eczema; skin epithelium; immune; infection; filaggrin
Categories
Funding
- NCATS NIH HHS [UL1 TR000154, UL1 TR001082] Funding Source: Medline
- NCRR NIH HHS [UL1 RR025780] Funding Source: Medline
- NIAID NIH HHS [HHSN272201000020I, HHSN272201000020C, U01 AI147462] Funding Source: Medline
- NIAMS NIH HHS [AR41256, R01 AR041256] Funding Source: Medline
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Atopic dermatitis (AD) is the most common chronic inflammatory skin disease. It often precedes the development of food allergy and asthma. Recent insights into AD reveal abnormalities in terminal differentiation of the epidermal epithelium leading to a defective stratum corneum, which allows enhanced allergen penetration and systemic IgE sensitization. Atopic skin is also predisposed to colonization or infection by pathogenic microbes, most notably Staphylococcus aureus and herpes simplex virus. Causes of this abnormal skin barrier are complex and driven by a combination of genetic, environmental, and immunologic factors. These factors likely account for the heterogeneity of AD onset and the severity and natural history of this skin disease. Recent studies suggest prevention of AD can be achieved through early interventions to protect the skin barrier. Onset of lesional AD requires effective control of local and systemic immune activation for optimal management. Early intervention might improve long-term outcomes for AD and reduce the systemic allergen sensitization that leads to associated allergic diseases in the gastrointestinal and respiratory tract.
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