Mechanisms of immune escape in the tumor microenvironment.

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Presentation transcript:

Mechanisms of immune escape in the tumor microenvironment. Mechanisms of immune escape in the tumor microenvironment. Several mechanisms, involving multiple immune components, contribute to tumor immune escape. (1) Immune recognition can be impaired following reduced expression of MHC class I molecules in malignant cells, resulting in decreased antigen presentation and consequently reduced detection by cytotoxic CD8+ T lymphocytes. (2) Cancer cells can activate immunosuppressive mechanisms by inducing immune cells' apoptosis through the expression of death signals (including FAS- and TRAIL-ligands). (3) Tumor cells release in the microenvironment a variety of immune-modulatory molecules that inhibit the immune system, such as IL6 and IL10, by inducing immunosuppressive Treg cells and MDSC, whereas the activity of cytotoxic CD8+ T cells and NK cells is inhibited. (4) This cytokine imbalance, combined with the secretion of TGFβ, COX-2, and PGE2, inhibits dendritic cell differentiation and maturation, thereby affecting antigen presentation and recognition by T cells. The release of additional immune modulators or metabolic regulators, such as IDO and arginase, also favors the establishment of an immunosuppressive tumor microenvironment. (5) Disrupted expression of immune checkpoint ligands by cancer cells provides coinhibitory signals to CD4+ and CD8+ T lymphocytes, preventing them from building a specific antitumor immune response. CCL, chemokine ligand; COX-2, cyclooxygenase-2; CXCL, chemokine (C-X-C motif) ligand; FAS-L, FAS-ligand; GM-CSF, granulocyte macrophage colony-stimulating factor; iDC, immature dentritic cell; IDO, indoleamine-2,3-deoxygenase; mDC, mature dentritic cell; MDSC, myeloid-derived suppressor cell; PD-1, programmed cell death 1; PD-L, programmed cell death ligand; PGE2, prostaglandin E2; TAN, tumor-associated neutrophil; TCR, T-cell receptor; Treg, regulatory T cells. Roman M. Chabanon et al. Clin Cancer Res 2016;22:4309-4321 ©2016 by American Association for Cancer Research