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Fig. 1 | Molecular Cancer

Fig. 1

From: Cross-talk between cancer stem cells and immune cells: potential therapeutic targets in the tumor immune microenvironment

Fig. 1

CSCs interfere with immune cell activity directly or through cytokines. CSCs suppress or evade antitumorigenic T cells in part by immune checkpoint (MHC-I, PD-L1 and CD80). CSCs reduce DCs mature and differentation via TGFβ and Ev (MHC-I, HLA-G). NKG2DL are able to kill MHC-I negative CSCs in an APC-independent manner. NK cells inhibitory ligands KIR2DL4 and NKG2A interact with HLA-G on CSCs and directly inhibits NK cells activation. CSCs further drive recruitment and polarization of TH17 cells and Treg cells by the combination of CCL-1, IL-2, IL-8, IL-10 and TGF-β1. Tregs produce TGF-β1 and IL-17 to promote self-renewal capacity, stem cell markers, and EMT toward tumor progression and invasion. CSCs also derived PD-L1 mediate the infiltration of Tregs. An additional layer of regulation of T cell activity is mediated indirectly by immunosuppressive myeloid cells, including macrophages and monocytic myeloid-derived suppressor cells (M-MDSCs). This effect partially depends on CSF1, CCL2, CCL5, TGF-β1 and PEG-E2 secreted by CSCs. The pathway of CSCs expressing TIM-3/Galectin 9 (Gal-9) expands the number of MDSCs. Exosome S100A9 enhances STAT3/NF-κB phosphorylation and production of prostaglandin E2 (PEG-E2) to promote CSCs. Collectively, these interactions reshape the tumour microenvironment and create a habitat where Treg cells and TH17 cells support CSCs, the latter via IL-17 production

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