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. 2022 Jul 4;13:927233. doi: 10.3389/fimmu.2022.927233

Figure 1.

Figure 1

The role of circulating neutrophils and neutrophils at the tumour site. Left: ① Glioma stem cells (GSCs) express S100A4 to promote the mesenchymal transition of glioma cells (37). ② The release of reactive oxygen species (ROS) by neutrophils in the early stage of glioma development may be related to the antitumour neutrophil effect (89). ③ Neutrophils secrete elastase, which destroys brain tissue and aids glioma invasion (90). Middle: ① Astrocytoma and GBM cells express IL-1 and TNF and high levels of IL-8 under alpha stimulation, which recruit neutrophils (91). ② Neutrophils form high-mobility group box 1 (HMGB1) and bind to receptor for advanced glycation end products (RAGE) expressed in glioma tissues, activates the NF-κB signaling pathway to secrete IL-8, and promote neutrophil infiltration (92). ③ Expression of FasL on glioma cells activates Fas signaling in the TME to express IL-8, leading to neutrophil aggregation (93). ④ LINC01116 promotes the expression of IL-1β by recruiting the transcription regulator DDX5 to the IL-1β promoter, which promotes the recruitment of neutrophils (94). ⑤ The ectopic expression of CD133 induces an increase in IL-1β expression, which causes neutrophils to aggregate in the TME (95). Right: Neutrophil degranulation and elevated levels of serum arginase I induce immunosuppression in GBM patients (96). Neutrophil expression of CD11b is an early predictor of tumour progression (97).