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Fig. 2 | Journal of Translational Medicine

Fig. 2

From: Avenues of research in dietary interventions to target tumor metabolism in osteosarcoma

Fig. 2

Cancer cell metabolism induces immunosuppression in the TME. Cancer cells compete with the host’s effector cells for nutrients. Their dysregulated metabolism leads to increased uptake of glucose and glutamine, depleting the effector cells from these nutrients, thus hindering their activity. Additionally, cancer cells release high amounts of lactate into the extracellular space, resulting in acidosis. This, in turn, makes the TME favorable for TILs, TAMs and MDSCs, and unsuitable for effector cells. TAMs are induced to express an M2 anti-inflammatory phenotype, secreting Il-10 and arginase. TILs also exhibit an anti-inflammatory phenotype, secreting Il-10 and TGF-β, while MDSC secrete Il-10, TGF-β and ROS. These factors further inhibit effector cells, promoting immunosuppression. TAM: Tumor-associated macrophages; IL-10: Interleukin-10; TGF-β: Transforming growth factor-β; ROS: Reactive oxygen species

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