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