De Benedetto Anna, Agnihothri Ritesh, McGirt Laura Y, Bankova Lora G, Beck Lisa A
Department of Dermatology, University of Rochester Medical Center, Rochester, New York 14642, USA.
J Invest Dermatol. 2009 Jan;129(1):14-30. doi: 10.1038/jid.2008.259.
Atopic dermatitis (AD) is a common chronic inflammatory skin disease that has increased in prevalence over the last half century. A growing body of evidence suggests that there are a variety of defects in the innate immune system that collectively affect the development and severity of AD. The reduction in antimicrobial peptides, diminished recruitment of innate immune cells (PMNs, pDC, and NK cells) to the skin, epithelial barrier disruption, and TLR2 defects are just some of the credible explanations for AD patients' susceptibility to pathogens such as Staphylococcus aureus, herpes simplex virus, and vaccinia virus. Although the focus for several years has been to identify defects in the innate immune system that might explain AD patients' susceptibility to cutaneous pathogens, it has become clear that some innate immune defects might promote inflammation and thereby aggravate or even induce the development of AD. Here we review the innate immune system, and highlight many of the potential innate networks that may be important in AD patients susceptible to cutaneous pathogens.
特应性皮炎（AD）是一种常见的慢性炎症性皮肤病，在过去半个世纪中患病率有所上升。越来越多的证据表明，先天性免疫系统存在多种缺陷，这些缺陷共同影响着AD的发生发展和严重程度。抗菌肽减少、先天性免疫细胞（中性粒细胞、浆细胞样树突状细胞和自然杀伤细胞）向皮肤的募集减少、上皮屏障破坏以及Toll样受体2（TLR2）缺陷，只是AD患者易感染金黄色葡萄球菌、单纯疱疹病毒和痘苗病毒等病原体的部分可信解释。尽管多年来的重点一直是确定先天性免疫系统中可能解释AD患者易患皮肤病原体的缺陷，但很明显，一些先天性免疫缺陷可能会促进炎症，从而加重甚至诱发AD的发生。在此，我们综述先天性免疫系统，并强调许多可能在易患皮肤病原体的AD患者中起重要作用的潜在先天性网络。
