Research progress on the neutrophil components and their interactions with immune cells in the development of psoriasis.

Abstract

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. We searched the recent literature on psoriasis and neutrophils through databases such as PubMed and CNKI, and summarized the findings to draw conclusions. 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). 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.