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. 2012 Jul 17;3:208. doi: 10.3389/fimmu.2012.00208

FIGURE 2.

FIGURE 2

Control of MDSC by cytokines. (A) Inflammatory environments lead to expansion of MDSC by activation of the STAT3 signaling pathway by several factors including granulocyte macrophage colony-stimulating factor (GM-CSF; Bronte et al., 1999); macrophage colony-stimulating factor (M-CSF; Kusmartsev et al., 2003); IL-6 (Bunt et al., 2007); peroxisome proliferator-activated receptor-gamma (PPARγ; Wu et al., 2012); vascular endothelial growth factor (VEGF; Ohm and Carbone, 2001; Melani et al., 2003); stem cell factor (SCF; Mellstedt et al., 1999); IL-13 (Gallina et al., 2006); Hps72 (Chalmin et al., 2010); and fms-like tyrosine kinase 3 ligand (Flt3L; Solheim et al., 2007). Agonists of the COX2 pathway also result in expansion of MDSC, including prostaglandin E2 (PGE2), lipopolysaccharide (LPS), IL-1β, and IFN-γ (Obermajer et al., 2011). The complement anaphylatoxin C5a is also described to induce MDSC (Markiewski et al., 2008). (B) Blockade of SCF/c-kit interaction or SCF blockade by siRNA reduce MDSC expansion (Mellstedt et al., 1999). The combination of IL-4 and GM-CSF inhibits MDSC function by inducing their differentiation into mature DC (Bronte et al., 1999; Sinha et al., 2007a).