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首页> 外文期刊>Clinics in dermatology >Abnormal epidermal barrier in the pathogenesis of atopic dermatitis
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Abnormal epidermal barrier in the pathogenesis of atopic dermatitis

机译：特应性皮炎发病机制中的表皮屏障异常

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Despite the acknowledged contributions of a defective epidermal permeability barrier, dryness of the skin, and the propensity to develop secondary infections to the etiology and pathophysiology of atopic dermatitis (AD), these epidermal changes have, until recently, been assumed to reflect downstream consequences that are secondary phenomena of the primary immunologic abnormality-the historical "inside-outside" view that AD is basically an intrinsic inflammatory disease.In this review, we focused on the role of the epidermal barrier function in the pathophysiology of AD. Specifically, we presented data in support of a barrier-initiated pathogenesis of AD, ie, the "outside-inside" concept. First, we reviewed the evidence on the existence of inherited barrier abnormalities in AD. Reported studies on the possible association of mutations in the filaggrin gene (. FLG) and data on human tissue kallikreins (KLKs) and AD have been addressed. We then dealt with the question of the causal link between impaired epidermal barrier and inflammation. Finally, the association between innate immune defense system and the increased avidity of . Staphylococcus aureus for atopic skin was examined.Despite very convincing evidence to support the barrier-initiated pathogenesis of AD, the view that AD reflects the downstream consequences of a primary immunologic abnormality cannot be dismissed out of hand. Almost every line of evidence in support of the role of the epidermal barrier as the "driver" of the disease activity can be challenged and at least partially contradicted by opposing evidence.Until more data are available and until all the dust settles around this issue, we should take advantage of what we already know and use our knowledge for practical purposes. Deployment of specific strategies to restore the barrier function in AD means the use of moisturizers as first-line therapy.
机译：尽管公认的表皮通透性障碍，皮肤干燥以及特应性皮炎（AD）的病因和病理生理发展为继发感染的可能性得到了公认，但直到最近，这些表皮的变化仍被认为反映了下游后果是原发性免疫学异常的继发现象-历史上从内而外的观点认为AD基本上是一种内在的炎症性疾病。在本文中，我们着重探讨了表皮屏障功能在AD病理生理中的作用。具体而言，我们提出了数据来支持AD的障碍引发的发病机制，即“由内而外”的概念。首先，我们回顾了有关AD中遗传性屏障异常的证据。已经报道了关于丝聚蛋白基因（.FLG）中突变的可能关联以及有关人类组织激肽释放酶（KLKs）和AD的数据的报道研究。然后，我们处理表皮屏障受损与炎症之间的因果关系问题。最后，先天性免疫防御系统与Aβ亲和力增加之间的关联。尽管有非常令人信服的证据支持AD的病原性发病机制，但仍不能一概而论地认为AD反映了原发性免疫异常的下游后果。几乎所有支持表皮屏障作为疾病活动“驱动器”作用的证据都可能受到对立证据的挑战，至少有部分矛盾。直到可获得更多数据，直到所有尘埃落定之前，我们应该利用我们已经知道的知识，并将我们的知识用于实际目的。部署用于恢复AD屏障功能的特定策略意味着要使用保湿剂作为一线疗法。

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