Update on the Pathogenesis and Therapy of Atopic Dermatitis
Update on the Pathogenesis and Therapy of Atopic Dermatitis
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特应性皮炎发病机制和治疗的最新进展
DOI：
10.1007/s12016-021-08880-3
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发表时间：
2021-08-02
影响因子：
9.1
通讯作者：
Yao, Zhirong
中科院分区：
文献类型：
--
作者：
Li, Huaguo;Zhang, Zhen;Yao, Zhirong
特应性皮炎(AD)是一种常见的炎症性皮肤病，以反复发作的湿疹和强烈的瘙痒为特征。虽然它通常在婴儿期开始并影响儿童，但它也在成年人中高度流行。在本文中，对AD的主要方面进行了更新，重点介绍了AD的发病和治疗方面。阿尔茨海默病的发病机制很复杂，很明显，强烈的遗传易感性、表皮功能障碍、皮肤微生物组异常、免疫失调和神经免疫系统在AD的发展中起着至关重要的作用。与表皮屏障破坏、夸大的病理性炎症和抗菌肽不足相关的基因突变可能会促进Th2炎症的增强，并介导瘙痒。目前对病原学的认识突出了肠道微生物多样性、NK细胞缺乏以及不同年龄和种族的不同免疫表型。对于轻度到重度AD的局部抗炎治疗，磷酸二酯酶4抑制剂(PDE-4)、JAK抑制剂和微生物群移植与Roseomonas粘膜提供了更多的治疗选择。中到重度AD的治疗仅限于症状和相对非特异性的免疫抑制方法。对阿尔茨海默病发病机制的深入了解导致了创新和靶向治疗的发展，如针对白介素4、白介素13和JAK/STAT抑制剂的生物制剂。其他潜在的AD治疗药物包括靶向T辅助细胞(Th)22和Th17/IL23途径的药物。对止痒治疗和益生菌补充治疗也进行了综述。
Atopic dermatitis (AD) is a common inflammatory skin disorder characterized by recurrent eczematous lesions and intense itch. Although it most often starts in infancy and affects children, it is also highly prevalent in adults. In this article, the main aspects of AD have been updated, with a focus on the pathogenetic and therapeutic aspects. The pathogenesis of AD is complex, and it is evident that a strong genetic predisposition, epidermal dysfunction, skin microbiome abnormalities, immune dysregulation, and the neuroimmune system are critical in AD development. Mutations in the genes associated with disrupted epidermal barrier, exaggerated pathological inflammation and inadequate antimicrobial peptides can promote enhanced Th2 inflammation and mediate pruritus. Current understanding of etiology highlights gut microbial diversity, NK cell deficiency, and different immunological phenotype with age and race. For topical anti-inflammatory treatment for mild-to-severe AD, phosphodiesterase 4 inhibitors (PDE-4), JAK inhibitors, and microbiome transplantation with Roseomonas mucosa provided more management selections. The treatment of moderate-to-severe AD has been limited to merely symptomatic and relatively nonspecific immunosuppressive approaches. In-depth understanding of the pathogenesis of AD has led to the development of innovative and targeted therapies, such as biologic agents targeting interleukin (IL)-4, IL-13 and JAK/STAT inhibitors. Other potential therapeutic agents for AD include agents targeting the T helper (Th) 22 and Th17/IL23 pathway. Antipruritic therapy and complementary probiotics therapy have also been reviewed.