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特应性皮炎和斑秃的重叠特征:从发病机制到治疗

Overlapping features of atopic dermatitis and alopecia areata: from pathogenesis to treatment.

作者信息

Cheng Jiayi, Jiang Yugu, Chen Qianqian, Xiao Min

机构信息

Department of Dermatology, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.

Department of Dermatology, The Affiliated Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.

出版信息

Front Immunol. 2025 Sep 3;16:1641918. doi: 10.3389/fimmu.2025.1641918. eCollection 2025.

DOI:10.3389/fimmu.2025.1641918
PMID:40969745
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12440913/
Abstract

Atopic dermatitis (AD) and alopecia areata (AA) have traditionally been regarded as inflammatory dermatoses with independent pathogenic mechanisms, with the former mostly categorized as a type 2 inflammatory disease and the latter as a type 1 inflammatory disease. However, immunologic studies have shown that the immunologic properties of AD and AA do not strictly follow the traditional classification. Both diseases are associated with systemic Th1, Th2, Th17, and Th22 cytokine imbalances, shared genetic susceptibility loci, overlapping immune pathways, and microbiome-mediated modulation of skin pathology. This review systematically investigates the intricate interactions between AD and AA, focusing on shared pathophysiologic mechanisms such as immune network crosstalk, metabolic dysregulation, and microbial influences. Furthermore, it critically evaluates current therapeutic strategies for overlapping disease manifestations, with a detailed analysis of emerging targeted therapies and their implications for clinical practice. By integrating existing evidence and identifying research gaps, this article aims to provide new perspectives on the understanding of the mechanisms of AD-AA interactions and to inform clinical decision-making and future research directions.

摘要

特应性皮炎(AD)和斑秃(AA)传统上被视为具有独立致病机制的炎症性皮肤病,前者大多归类为2型炎症性疾病,后者归类为1型炎症性疾病。然而,免疫学研究表明,AD和AA的免疫学特性并不严格遵循传统分类。这两种疾病都与全身性Th1、Th2、Th17和Th22细胞因子失衡、共同的遗传易感性位点、重叠的免疫途径以及微生物群介导的皮肤病理调节有关。本综述系统地研究了AD和AA之间的复杂相互作用,重点关注免疫网络串扰、代谢失调和微生物影响等共同的病理生理机制。此外,本综述批判性地评估了针对重叠疾病表现的当前治疗策略,并详细分析了新兴的靶向治疗方法及其对临床实践的影响。通过整合现有证据并找出研究差距,本文旨在为理解AD-AA相互作用机制提供新的视角,并为临床决策和未来研究方向提供参考。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/251e/12440913/4bab244cf44e/fimmu-16-1641918-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/251e/12440913/88374c7582cf/fimmu-16-1641918-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/251e/12440913/410db500d290/fimmu-16-1641918-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/251e/12440913/23056f2bbc3c/fimmu-16-1641918-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/251e/12440913/4bab244cf44e/fimmu-16-1641918-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/251e/12440913/88374c7582cf/fimmu-16-1641918-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/251e/12440913/410db500d290/fimmu-16-1641918-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/251e/12440913/23056f2bbc3c/fimmu-16-1641918-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/251e/12440913/4bab244cf44e/fimmu-16-1641918-g004.jpg

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