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. Author manuscript; available in PMC: 2013 Jul 5.
Published in final edited form as: Semin Cancer Biol. 2012 Feb 1;22(4):275–281. doi: 10.1016/j.semcancer.2012.01.011

Fig. 2.

Fig. 2

Inflammation enhances MDSC–macrophage cross-talk. Tumor and stromal cells within the tumor microenvironment secrete a variety of inflammatory mediators. For example, tumor cells produce PGE2 which activates MDSC through the EP receptors and COX2 which promotes the production of PGE2 from arachidonic acid. Tumor cells and MDSC produce VEGF, IL-6 and S100A8/A9 proteins which bind to their respective receptors on MDSC, as well as IL-1β which acts via IL-6. These mediators accentuate the cross-talk between MDSC and macrophages and further increase MDSC production of IL-10 and decrease macrophage production of IL-12. Inflammation-increased MDSC production of IL-10 is TLR4-dependent and involves up-regulation of CD14.