IL1B and glioma: Multiple chemokines, e.g., pro-inflammatory factors (IL-1β, IL-6), activated T cell-derived cytokines (IFN-γ, IL-4, IL-10, and IL-13) and multiple soluble mediators secreted by gliomas (granulocyte macrophage [GM]-CSF, vascular endothelial growth factor [VEGF], PGE-2, and TGF-β2), attract MDSCs toward the tumor and synergistically initiate immunosuppressive pathways that commit immature myeloid cells to become MDSCs; this then further promotes the differentiation of MDSCs toward TAMs (78–80).