Skewed Signaling through the Receptor for Advanced Glycation End-Products Alters the Proinflammatory Profile of Tumor-Associated Macrophages

摘要: Tumors are complex tissues composed of variable amounts both non-cellular components (matrix proteins) and a multitude stromal cell types, which under an active cross-talk with tumor cells. Tumor-associated macrophages (TAMs) the major leukocyte population among tumor-infiltrating immune Once they infiltrated into stroma undergo polarized activation, where M1 M2 phenotypes represent two extreme polarization heterogeneity spectrum. It is known that TAMs acquire specific phenotype (M2), oriented toward growth, angiogenesis immune-suppression. A growing body evidences supports presence tuning mechanisms in order to skew or restraint inflammatory response thus forces them function as tumor-promoting The receptor advanced glycation end-products (RAGE) member immunoglobulin protein family surface molecules, being activated by several danger signals signaling promote production many pro-inflammatory molecules. Interestingly, this paradoxically expressed phenotypes. This review addresses how RAGE has been drifted away macrophages, taking advantage abundance ligands at microenvironment, particularly HMGB1, reinforce supportive strategy support growth.