Wollenberg Andreas, Klein Elisabeth
Department of Dermatology and Allergy, Ludwig-Maximilian-University of Munich, Frauenlobstr 9-11, 80337, Munich, Germany.
Clin Rev Allergy Immunol. 2007 Oct;33(1-2):35-44. doi: 10.1007/s12016-007-0032-9.
Atopic dermatitis (AD) is a highly pruritic, chronic, multifactorial skin disease predisposing to bacterial and viral infections based on abnormalities of the innate and acquired immune system. The innate system quickly mobilizes an inflexible, standardized first-line response against different pathogens. Epidermal barrier dysfunction results in increased protein allergen penetration through the epidermis and predisposes to secondary skin infections. Two loss-of-function mutations in the epidermal filaggrin gene are associated with AD. Langerhans cells and inflammatory dendritic epidermal cells (IDEC) express high affinity IgE receptors, which are functional in IgE-mediated antigen presentation. Inducible antimicrobial peptides including the antiviral cathelicidin and the antibacterial beta-defensins show defective upregulation in lesional AD skin. The desmosomal protein nectin-1 is unmasked in AD lesions, thus becoming a relevant herpes simplex virus (HSV) entry receptor. Type I IFN-producing plasmacytoid dendritic cells are decreased and dysfunctional in AD skin, predisposing the patients to viral skin infections. Molluscum contagiosum virus produces a unique IL-18 binding protein to evade antiviral defense mechanisms. Innate and adaptive immunity do not simply coexist but are linked to one another in a complex network of skin immunobiology.
特应性皮炎（AD）是一种高度瘙痒的慢性多因素皮肤病，基于先天性和获得性免疫系统异常，易引发细菌和病毒感染。先天性免疫系统会迅速动员针对不同病原体的固定、标准化一线反应。表皮屏障功能障碍导致蛋白质过敏原通过表皮的渗透增加，并易引发继发性皮肤感染。表皮丝聚合蛋白基因的两个功能丧失突变与特应性皮炎有关。朗格汉斯细胞和炎症性树突状表皮细胞（IDEC）表达高亲和力IgE受体，其在IgE介导的抗原呈递中发挥作用。包括抗病毒的cathelicidin和抗菌的β-防御素在内的可诱导抗菌肽在AD皮损中上调存在缺陷。桥粒蛋白nectin-1在AD皮损中暴露，从而成为相关单纯疱疹病毒（HSV）的进入受体。产生I型干扰素的浆细胞样树突状细胞在AD皮肤中减少且功能失调，使患者易患病毒性皮肤感染。传染性软疣病毒产生独特的IL-18结合蛋白以逃避抗病毒防御机制。先天性免疫和适应性免疫并非简单共存，而是在皮肤免疫生物学的复杂网络中相互关联。
