银屑病
免疫系统
免疫学
发病机制
趋化性
中性粒细胞胞外陷阱
医学
生物
炎症
受体
遗传学
作者
Zhenhui Wang,Dongmei Shi
摘要
BACKGROUND: Psoriasis is an immune-mediated chronic inflammatory disease, and currently it is widely believed that the IL-23/IL-17 axis and Th17 cells play a critical and central role. However, increasing evidence suggests that neutrophils may interact with a variety of immune cells to play an indispensable role in psoriasis. MATERIALS AND METHODS: We searched the recent literature on psoriasis and neutrophils through databases such as PubMed and CNKI, and summarized the findings to draw conclusions. RESULTS: Neutrophils can promote the development of psoriasis by secreting IL-23, IL-17, and cytokines with TH17 cell chemotaxis. Activated keratinocytes (KCs) can attract and activate neutrophils, induce the formation of neutrophil extracellular traps (NETs). KCs can also expose self-antigens which lead to strong autoimmune reactions. The granule proteins secreted by activated neutrophils can activate IL-36, which converts vulgaris psoriasis to generalized pustular psoriasis (GPP). CONCLUSION: The function of neutrophils components and the interaction between neutrophils and immune cells play an essential role in the pathogenesis of psoriasis. The aim is to provide a theoretical basis for the exploration of targeted clinical treatments and fundamental research on the pathogenesis of psoriasis.
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