PDF(Pubmed)
Abstract：
Atopic dermatitis (AD) is a chronic, relapsing immunoinflammatory skin condition characterized by sensations such as pruritis, pain, and neuronal hypersensitivity. The mechanisms underlying these sensations are multifactorial and involve complex crosstalk among several cutaneous components. This review explores the role these components play in the pathophysiology of atopic dermatitis. In the skin intercellular spaces, sensory nerves interact with keratinocytes and immune cells via myriad mediators and receptors. These interactions generate action potentials that transmit pruritis and pain signals from the peripheral nervous system to the brain. Keratinocytes, the most abundant cell type in the epidermis, are key effector cells, triggering crosstalk with immune cells and sensory neurons to elicit pruritis, pain, and inflammation. Filaggrin expression by keratinocytes is reduced in atopic dermatitis, causing a weakened skin barrier and elevated skin pH. Fibroblasts are the main cell type in the dermis and, in atopic dermatitis, appear to reduce keratinocyte differentiation, further weakening the skin barrier. Fibroblasts and mast cells promote inflammation while dermal dendritic cells appear to attenuate inflammation. Inflammatory cytokines and chemokines play a major role in AD pathogenesis. Type 2 immune responses typically generate pruritis, and the type 1 and type 3 responses generate pain. Type 2 responses and increased skin pH contribute to barrier dysfunction and promote dysbiosis of the skin microbiome, causing the proliferation of Staphyloccocus aureus. In conclusion, understanding the dynamic interactions between cutaneous components in AD could drive the development of therapies to improve the quality of life for patients with AD.
摘要：
特应性皮炎(AD)是一种慢性、以瘙痒等感觉为特征的复发性免疫炎症性皮肤病，疼痛,和神经元超敏反应。这些感觉的潜在机制是多因素的，并且涉及几种皮肤成分之间的复杂串扰。这篇综述探讨了这些成分在特应性皮炎的病理生理学中的作用。在皮肤细胞间隙中，感觉神经通过多种介质和受体与角质形成细胞和免疫细胞相互作用。这些相互作用产生动作电位，将瘙痒和疼痛信号从周围神经系统传递到大脑。角质形成细胞,表皮中最丰富的细胞类型，是关键的效应细胞，触发与免疫细胞和感觉神经元的串扰引发瘙痒，疼痛,和炎症。在特应性皮炎中，角质形成细胞的聚丝蛋白表达减少，导致皮肤屏障减弱和皮肤pH值升高。成纤维细胞是真皮中的主要细胞类型,在特应性皮炎中，似乎减少角质形成细胞分化，进一步削弱皮肤屏障。成纤维细胞和肥大细胞促进炎症，而真皮树突状细胞似乎减轻炎症。炎性细胞因子和趋化因子在AD病发机制中起主要感化。2型免疫反应通常会产生瘙痒，1型和3型反应产生疼痛。2型反应和增加的皮肤pH有助于屏障功能障碍和促进皮肤微生物群的生态失调，引起金黄色葡萄球菌的增殖。总之,了解AD中皮肤成分之间的动态相互作用可以推动治疗方法的发展,以改善AD患者的生活质量.
