中性粒细胞与特应性皮炎：从病理机制到研究进展

doi:10.12372/jcp.2026.25e1601

摘要/Abstract

摘要：

特应性皮炎（AD）是一种由多因素介导的慢性复发性炎症性皮肤病，免疫应答异常为其核心发病机制。固有免疫细胞是AD皮肤早期炎症反应核心，并可作为关键的炎症信号传导与放大节点。中性粒细胞（NEU）作为固有免疫的核心细胞，在炎症发生和抗菌免疫中有重要作用。本文对目前 NEU 的来源、分类、活化机制及促炎、免疫抑制、非典型性等生理病理功能进行了概述，并探讨其如何在感受到皮肤炎症或抗原信号后迅速活化，随后通过趋化、脱颗粒、胞吞作用、产生活性氧和形成中性粒细胞胞外诱捕网（NETs）等效应机制促进炎症进展，招募其他免疫细胞共同参与皮肤屏障损伤以及瘙痒感觉的形成机制。本文旨在全面展示关于NEU参与AD病理生理进程的前沿观点，以帮助读者掌握这一领域的研究进展。

关键词: 中性粒细胞, 特应性皮炎, 炎症, 瘙痒

Abstract:

Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disorder driven by multifactorial mechanisms, with dysregulated immune responses as its central pathogenesis. Innate immune cells serve as the core of early inflammatory reactions in AD skin and act as critical nodes for inflammatory signal transduction and amplification. Neutrophils (NEU), the pivotal cellular component of innate immunity, play essential roles in the initiation of inflammation and antibacterial immunity. This review provides an overview of the current understanding regarding the origin, classification, activation mechanisms, and physiological/pathological functions of NEU—including pro-inflammatory, immunosuppressive, and atypical properties. It further explores how NEU rapidly activate upon sensing cutaneous inflammatory or antigenic signals, and subsequently promote inflammatory progression through effector mechanisms such as chemotaxis, degranulation, phagocytosis, reactive oxygen species (ROS) production, and formation of neutrophil extracellular traps (NETs). Additionally, NEU recruit other immune cells to collectively contribute to the development of skin barrier impairment and pruritus. This review aims to comprehensively present cutting-edge insights into the involvement of NEU in the pathophysiological processes of AD, thereby facilitating readers' grasp of research advances in this field.

Key words: neutrophil, atopic dermatitis, inflammation, pruritus

中图分类号:

唐淇钧, 罗晓燕. 中性粒细胞与特应性皮炎：从病理机制到研究进展[J]. 临床儿科杂志, 2026, 44(5): 405-411.

TANG Qijun, LUO Xiaoyan. Neutrophils and atopic dermatitis: from pathological mechanisms to research advances[J]. Journal of Clinical Pediatrics, 2026, 44(5): 405-411.

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