Fig. 3
From: Immunobiology of cancer-associated fibroblasts in the context of radiotherapy
Cancer-associated fibroblasts (CAFs) maintain their immunosuppressive phenotype following exposure to ionizing radiation (IR). Radiation treatment by IR is able to induce weighty changes in the phenotype of CAFs, however recent studies have demonstrated that CAFs retain their immunosuppressive functions over different innate and adaptive immune cells after radiation treatment. The release of key immunoregulators remain constant in radiation-induced senescent CAFs. In contrast to what has been observed with tumor cells, CAFs do not undergo immunogenic cell death (ICD) and do not activate interferon type 1 (IFN-1) responses following radiation, while expression of some inhibitory surface receptors is enhanced. CCL2 chemokine (C–C motif) ligand 2; CHI3L1 chitinase-3 like protein 1; CD73 cluster-of-differentiation-73; CTL cytotoxic T lymphocytes; DC dendritic cells; FasL Fas (or CD95) ligand; GM-CSF granulocyte–macrophage colony-stimulating factor; ICD immunogenic cell death; IDO Indoleamine-2,3-dioxygenase; IFN-1 type I interferon; IL-6 interleukin-6; Mø Macrophages; M2-MØs (anti-inflammatory) type-2 macrophages; NK cell natural killer cell; PD-L1 programmed death ligand-1; PGE2 prostaglandin E2; TDO2 tryptophan 2,3-dioxygenase; tDC tolerogenic dendritic cell; TSLP thymic stromal lymphopoietin; TGFb transforming growth factor beta. Schematic created by BioRender