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Update on the Pathogenesis and Therapy of Atopic Dermatitis
Clinical Reviews in Allergy & Immunology ( IF 8.4 ) Pub Date : 2021-08-02 , DOI: 10.1007/s12016-021-08880-3
Huaguo Li 1, 2 , Zhen Zhang 1, 2 , Hui Zhang 1, 2 , Yifeng Guo 1, 2 , Zhirong Yao 1, 2
Affiliation  

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.



中文翻译:

特应性皮炎的发病机制和治疗更新

特应性皮炎 (AD) 是一种常见的炎症性皮肤病,其特征是反复出现湿疹性病变和剧烈瘙痒。虽然它最常开始于婴儿期并影响儿童,但它在成人中也非常普遍。在本文中,更新了 AD 的主要方面,重点是发病机制和治疗方面。AD 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 发展中至关重要。与表皮屏障破坏、病理性炎症过度和抗菌肽不足相关的基因突变可促进 Th2 炎症增强并介导瘙痒。目前对病因的理解突出了肠道微生物的多样性,NK 细胞缺乏,以及不同年龄和种族的免疫表型。对于轻度至重度 AD 的局部抗炎治疗,磷酸二酯酶 4 抑制剂 (PDE-4) JAK 抑制剂和使用粘膜玫瑰单胞菌进行微生物组移植提供了更多的管理选择。中度至重度 AD 的治疗仅限于仅对症和相对非特异性的免疫抑制方法。对 AD 发病机制的深入了解导致了创新和靶向疗法的发展,例如靶向白细胞介素 (IL)-4、IL-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 通路的药物。止痒疗法和补充益生菌疗法也进行了审查。

更新日期:2021-08-02
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