1. Figure 1 Radiation-induced effects on tumour cells
Figure 1 | Radiation-induced effects on tumour cells. Ionizing radiation initiates: (1) cell death, (2) cytokine and chemokine production in the tumour microenvironment, (3) release of tumour antigens, (4) release of DAMPs, (5) recruitment of IL-1β, TGFβ, FGF, TNF, and NLRP-3, and (6) the generation of chemotactic signals that recruit several myeloid cell populations with distinct roles in T-cell suppression. These primary events are the catalysts for an elaborate succession of processes. Cell death (1) causes the release of DNA and RNA into the cytoplasm leading to the production of IFN. Cytokine and chemokine production (2) triggers the infiltration of DCs, macrophages, cytotoxic T cells, regulatory T cells, and MDSCs, as well as the efflux of immune cells. The release of DAMPs (4) activates APCs. These complex and sometimes conflicting events are reflective of the struggle between host immune response and tumour prosurvival mechanisms. APCs, antigen-presenting cells; cGAMP, cyclic GMP-AMP; cGAS, cyclic GMP-AMP synthase; DAMPs, damage-associated molecular patterns; DC, dendritic cell; FGF, fibroblast growth factor; HMGB1, high mobility group protein B1; IFN, interferon; IL-1β, interleukin 1β; IL-10, interleukin 10; MDSC, myeloid-derived suppressor cells; NLRP3; NACHT, LRR and PYD domains-containing protein 3; PD-L1, programmed cell death 1 ligand 1; RLRs, RIG-I-like receptors; STING, stimulator of interferon genes; TGFβ, transforming growth factor-β; TLRs, Toll-like receptors; TNF, tumour necrosis factor; Treg cells, regulatory T cells.
Weichselbaum, R. R. et al. (2017) Radiotherapy and immunotherapy: a beneficial liaison?
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