免疫学
嗜碱性粒细胞
医学
特应性皮炎
免疫系统
敏化
炎症
发病机制
过敏
嗜碱性粒细胞活化
免疫球蛋白E
过敏反应
肥大细胞
过敏性炎症
获得性免疫系统
先天免疫系统
全身炎症
电池类型
渗透(HVAC)
疾病
嗜酸性粒细胞
胸腺基质淋巴细胞生成素
作者
Mrinmoy Das,Raif S. Geha
出处
期刊:PubMed
日期:2025-11-15
标识
DOI:10.1016/j.anai.2025.11.005
摘要
Atopic dermatitis (AD) or eczema is a chronic inflammatory skin disease, characterized by dysfunction of the epidermal skin barrier causing increased sensitization to environmental allergens. The resulting type 2-dominated local and systemic immune response causes epidermal hyperplasia, dermal infiltration by T cells and eosinophilia, and elevated levels of total and allergen-specific IgE. In addition, the skin of AD patients is often colonized with Staphylococcus aureus which correlates with diseases severity. Recent emerging studies highlights a significant role for basophils in both local and systemic response of AD pathogenesis. Although rare in the circulation, basophils rapidly infiltrate inflamed skin and upon activation, they release IL-4 and IL-13, which are key players in the development of AD. They also secrete mediators like histamine, leukotrienes and IL-31 that contribute to inflammation and pruritus. Basophils also influence through their production of IL-4 T cell polarization, and B cell class switching, supporting systemic sensitization and the development of atopic march. Basophils are gaining recognition as clinically actionable contributors to AD. The basophil activation test, which measures the activation of basophils in blood in response to specific allergens offers promising tools for assessing AD pathogenesis and response to treatment. Additionally, therapies such as dupilumab, tralokinumab, and nemolizumab which target IL-4, IL-13 and IL-31 respectively, likely exert part of their effect by modulating basophil activity. In this review, we summarize the immunologic functions of basophils in AD pathogenesis, discuss their relevance as biomarkers and therapeutic targets, and outline future directions for integrating basophil-focused strategies in the management of patients with AD.
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