Fig. 2.

Changes in the TME of HCC before and after radiotherapy. TME of HCC before radiotherapy. (1) In the context of persistent chronic inflammation, activated Kupffer cells (KCs) release CCL2 while recruiting inflammatory monocytes and MDSCs and promoting HCC progression. (2) Tumour cell production of CCL5 and CCL2 promotes the infiltration of MDSCs and Tregs, which in turn inhibits the production of CD8+ T cells and immunosuppressive transforming growth factor β (TGF-β). (3) M2-like TAMs secrete interleukin 1β(IL-1β), IL-6, TNF, CCL2, and CXCL10, which promote the proliferation of tumour cells and are associated with poor patient prognosis. Radiotherapy reshapes the TME of HCC. (1) Radiotherapy induces the upregulated expression of MHC-I on the surface of tumour cells, which promotes the maturation of DCs and the presentation of tumour-associated antigens. Mature DCs release CXCL9 and CXCL10 to promote the infiltration of CD8+ T-cells in the TME. (2) Radiotherapy induces tumour cells to secrete CXCL16, which further promotes the activation and expansion of CD8+ T-cells