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. 2022 Dec 13;23(24):15827. doi: 10.3390/ijms232415827

Figure 1.

Figure 1

Neutrophil heterogeneity during tumor development. In the peripheral blood of cancer patients, three distinct populations of circulating neutrophils can be found: NDNs, LDNs, and g-MDSCs. Tumors recruit neutrophils via various mediators. These mediators include G-CSF [19], CXCL1 [20], CXCL2 [21], CXCL5 [22], CXCL8 [23], CXCL12 [24], IL-10 [19], IL-17 [25], and TGF-β [26]. After infiltration into the tumor microenvironment, neutrophils gain an N1 or N2 phenotype under the action of IFN-β [27] or TGF-β [14], respectively. Neutrophils in their turn reshape the tumor microenvironment: N1 TANs secrete pro-inflammatory anti-tumor mediators [14,28], while N2 TANs support tumor progression and angiogenesis and enhance the immunosuppressive tumor microenvironment [24,28]. NDNs—normal-density neutrophils, LDNs—low-density neutrophils, g-MDSCs—granulocytic-myeloid-derived suppressor cells, G-CSF—granulocyte colony-stimulating factor, CXCL—C-X-C motif chemokine ligand, CCL—C-C motif chemokine ligand, IL—interleukin, TGF-β—transforming growth factor beta, IFN-β—interferon beta, TNF-α—tumor necrosis factor alpha, ROS—reactive oxygen species, VEGF—vascular endothelial growth factor, MMP9—matrix metallopeptidase 9, TME—tumor microenvironment.