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Fig. 1 | Journal for ImmunoTherapy of Cancer

Fig. 1

From: Unfolding anti-tumor immunity: ER stress responses sculpt tolerogenic myeloid cells in cancer

Fig. 1

Hostile conditions in the tumor microenvironment such as hypoxia, nutrient deprivation and ROS can provoke ER stress and trigger the UPR in various tumor-resident cell types. Intrinsic ER stress responses in cancer cells ensure their survival under hypoxic conditions, increase expression of pro-angiogenic factors, promote metastasis and inhibit the presentation of their own antigens. Myeloid-intrinsic ER stress responses mediate reprogramming towards immunosuppressive and tolerogenic phenotypes. Induction of ER stress in myeloid cells may occur via transmissible factors released by ER-stressed cancer cells in the same milieu. Intracellular generation and accumulation of lipid peroxidation byproducts can further elicit intrinsic ER stress responses in myeloid cells. ER stress sensors therefore emerge as attractive targets for developing new immunotherapeutic approaches that may synergize with standard cancer treatments

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