Yue Chengcheng, Zhou Hong, Wang Xiaoyan, Yu Jiadong, Hu Yawen, Zhou Pei, Zhao Fulei, Zeng Fanlian, Li Guolin, Li Ya, Feng Yuting, Sun Xiaochi, Huang Shishi, He Mingxiang, Wu Wenling, Huang Nongyu, Li Jiong
State Key Laboratory of Biotherapy and Cancer Center West China Hospital Sichuan University Sichuan University and Collaborative Innovation Center for Biotherapy Chengdu Sichuan China.
Department of Cardiology West China Hospital Sichuan University Chengdu Sichuan China.
MedComm (2020). 2024 Dec 8;5(12):e70029. doi: 10.1002/mco2.70029. eCollection 2024 Dec.
The skin serves as the first protective barrier for nonspecific immunity and encompasses a vast network of skin-associated immune cells. Atopic dermatitis (AD) is a prevalent inflammatory skin disease that affects individuals of all ages and races, with a complex pathogenesis intricately linked to genetic, environmental factors, skin barrier dysfunction as well as immune dysfunction. Individuals diagnosed with AD frequently exhibit genetic predispositions, characterized by mutations that impact the structural integrity of the skin barrier. This barrier dysfunction leads to the release of alarmins, activating the type 2 immune pathway and recruiting various immune cells to the skin, where they coordinate cutaneous immune responses. In this review, we summarize experimental models of AD and provide an overview of its pathogenesis and the therapeutic interventions. We focus on elucidating the intricate interplay between the immune system of the skin and the complex regulatory mechanisms, as well as commonly used treatments for AD, aiming to systematically understand the cellular and molecular crosstalk in AD-affected skin. Our overarching objective is to provide novel insights and inform potential clinical interventions to reduce the incidence and impact of AD.
皮肤是天然免疫的第一道保护屏障，包含一个庞大的皮肤相关免疫细胞网络。特应性皮炎（AD）是一种常见的炎症性皮肤病，影响所有年龄和种族的人群，其发病机制复杂，与遗传、环境因素、皮肤屏障功能障碍以及免疫功能障碍密切相关。被诊断为AD的个体通常具有遗传易感性，其特征是影响皮肤屏障结构完整性的突变。这种屏障功能障碍导致警报素释放，激活2型免疫途径并将各种免疫细胞招募到皮肤，在那里它们协调皮肤免疫反应。在这篇综述中，我们总结了AD的实验模型，并概述了其发病机制和治疗干预措施。我们专注于阐明皮肤免疫系统与复杂调节机制之间的复杂相互作用，以及AD的常用治疗方法，旨在系统地了解AD患者皮肤中的细胞和分子相互作用。我们的总体目标是提供新的见解，并为潜在的临床干预措施提供参考，以降低AD的发病率和影响。
