Author(s): Ong PY
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Abstract It is known that Staphylococcus aureus induces the expression of human beta-defensin-2 (hBD-2), a well-characterized antimicrobial peptide, in keratinocytes. However, in spite of heavy colonization of atopic dermatitis (AD) skin lesions by S. aureus, these lesions have consistently been shown to contain low expression of hBD-2. The current article discusses various possible mechanisms for the low expression of hBD-2 in AD and raises the question whether the innate recognition of S. aureus by keratinocytes in AD is intact. Copyright (c) 2006 S. Karger AG, Basel.
This article was published in Dermatology
and referenced in Journal of Clinical & Cellular Immunology