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. 2017 Mar 27;7(2):34. doi: 10.3390/biom7020034

Figure 1.

Figure 1

Inflammatory microenvironment prevalent in brain cancers. The glioma microenvironment is heavily infiltrated with different inflammatory cells, including microglia, macrophage, neutrophil, eosinophil, monocytes, dendritic cells, T-cells, B-cells, and myeloid derived suppressor cells (MDSCs) [18]. Upon activation, these cells release an array of mediators that promote cancer cell proliferation, survival, migration and invasion. These include the pro-inflammatory and cytotoxic cytokines, growth factors, bioactive lipids, hydrolytic enzymes, matrix metalloproteinases, reactive oxygen intermediates, and nitric oxide [19,20]. The cell types involved and the cytokines produced are shown. CCL: C–C Motif Chemokine Ligand 2/monocyte chemoattractant protein 1 (MCP1); TNF-α: Tumor necrosis factor-alpha; CXCL: Chemokine (C–X–C motif) ligand; INF-ɣ: Interferon gamma; TAM: Tumor-associated macrophages; Tregs: Regulatory T-cells; IL-1β: Interleukin 1 beta; IL-2/6/10/12: Interleukin 2/6/10/12; CSF-1: Colony stimulating factor 1; GM-CSF: Granulocyte-macrophage colony-stimulating factor; HGF/SF: Hepatocyte growth factor or scatter factor; SDF-1: Stromal cell-derived factor 1; MCP-1/3 : Monocyte chemoattractant protein 1 or 3; GDNF: Glial cell-derived neurotrophic factor; TGF-β: Transforming growth factor beta; EGF: Epidermal growth factor; STI1: Stress inducible protein 1; MT1-MMP: Membrane type 1-matrix metalloproteinase; MMP2/9: Matrix metalloproteinase 2 or 9.