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.
Keywords: granule proteins; neutrophil; neutrophil extracellular traps; psoriasis.
© 2023 The Authors. Skin Research and Technology published by John Wiley & Sons Ltd.