Levin Jacquelyn, Friedlander Sheila Fallon, Del Rosso James Q
Dr. Levin is from Largo Medical Center, Largo, Florida. Dr. Friedlander is from University Of California San Diego, San Diego, California. Dr. Del Rosso is from Valley Hospital Medical Center, Las Vegas, Nevada.
J Clin Aesthet Dermatol. 2013 Nov;6(11):49-54.
This three-part review presents what is currently known about the involvement and interdependency of the epidermal barrier and immune response in the etiopathogenesis of atopic dermatitis. Part 1 of this review depicted the role of filaggrin in atopic dermatitis while this article, Part 2, evaluates the role of serine proteases and specific lipids in the structural and functional integrity of the stratum corneum and its multiple barrier functions in atopic dermatitis. Upregulation of serine protease activity causes adverse structural changes of the stratum corneum due to degradation of certain stratum corneum proteins that are integral to epidermal structure and functions, interference with the formation of the stratum corneum intercellular lipid membrane, which normally regulates epidermal water flux and gradient, and induction of a TH2 pattern of inflammation, which is the hallmark profile of atopic skin. Alteration in lipid ratios and changes in lipid-directed enzymes may play a role in the impairment of barrier functions that are associated with atopic dermatitis. In Part 3, immune dysregulation, including upregulation of a TH2 inflammation pattern, augmented allergic sensitization, sustained wound healing inflammation, and impaired innate immunity are discussed. The roles of the stratum corneum permeability barrier, the immune defense barrier, and antimicrobial barrier in AD pathogenesis are explained in detail. With this explanation, the interdependence of the multitude of polymorphisms and dysregulations seen in AD skin will become clear. The condensing of these impaired and/or dysregulated functions and how they interact should provide further knowledge about the pathogenic mechanisms that cause atopic dermatitis, how they are clinically relevant, and how they may assist in developing more specific therapies directed at the pathogenesis of atopic dermatitis.
这篇分为三个部分的综述介绍了目前已知的表皮屏障与免疫反应在特应性皮炎发病机制中的参与情况和相互依存关系。本综述的第1部分描述了丝聚蛋白在特应性皮炎中的作用,而本文作为第2部分,评估了丝氨酸蛋白酶和特定脂质在特应性皮炎中角质层结构和功能完整性及其多种屏障功能中的作用。丝氨酸蛋白酶活性上调会导致角质层出现不良结构变化,原因包括某些对表皮结构和功能至关重要的角质层蛋白降解、干扰正常调节表皮水分通量和梯度的角质层细胞间脂质膜形成,以及诱导特应性皮肤的标志性炎症模式即TH2炎症模式。脂质比例的改变和脂质导向酶的变化可能在与特应性皮炎相关的屏障功能受损中起作用。在第3部分中,将讨论免疫失调,包括TH2炎症模式上调、过敏致敏增强、伤口愈合炎症持续以及先天免疫受损。详细解释了角质层渗透屏障、免疫防御屏障和抗菌屏障在特应性皮炎发病机制中的作用。通过这种解释,特应性皮炎皮肤中多种多态性和失调之间的相互依存关系将变得清晰。这些受损和/或失调功能的浓缩以及它们如何相互作用,应该能提供更多关于导致特应性皮炎的致病机制、它们在临床上的相关性以及它们如何有助于开发针对特应性皮炎发病机制的更特异性疗法的知识。