特应性皮炎中金黄色葡萄球菌的模式识别受体是否存在缺陷？
Is/are pattern recognition receptor(s) for Staphylococcus aureus defective in atopic dermatitis?
作者信息
Ong Peck Y
机构信息
Division of Clinical Immunology/Allergy, Department of Pediatrics, Childrens Hospital Los Angeles/Keck School of Medicine, University of Southern California, Los Angeles, CA 90027, USA.
出版信息
Dermatology. 2006;212(1):19-22. doi: 10.1159/000089016.
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.
已知金黄色葡萄球菌可诱导角质形成细胞中人类β-防御素2（hBD-2，一种特征明确的抗菌肽）的表达。然而，尽管金黄色葡萄球菌在特应性皮炎（AD）皮肤病变中大量定植，但这些病变一直被证明hBD-2表达较低。本文讨论了AD中hBD-2低表达的各种可能机制，并提出了AD中角质形成细胞对金黄色葡萄球菌的天然识别是否完整的问题。
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