Tumor microenvironment (TME) includes a wide range of cell types including cancer cells, cells which are involved in stromal structure and immune cells (tumor suppressor and tumor promoting cells). These cells have several interactions with each other that are mainly regulated via the release of intercellular mediators. Radiotherapy can modulate these interactions via shifting secretions into inflammatory or anti-inflammatory responses. Radiotherapy also can trigger resistance of cancer (stem) cells via activation of stromal cells. The main mechanisms of tumor resistance to radiotherapy is the exhaustion of anti-tumor immunity via suppression of CD4+ T cells and apoptosis of cytotoxic CD8+ T lymphocytes (CTLs). Cancer-associated fibroblasts (CAFs), mesenchymal-derived suppressor cells (MDSCs) and regulatory T cells (Tregs) are the main suppressor of anti-tumor immunity via the release of several chemokines, cytokines and immune suppressors. In this review, we explain the main cellular and molecular interactions and secretions in TME following radiotherapy. Furthermore, the main signaling pathways and intercellular connections that can be targeted to improve therapeutic efficiency of radiotherapy will be discussed.

肿瘤微环境（TME）包括多种细胞类型，包括癌细胞，参与基质结构的细胞和免疫细胞（肿瘤抑制细胞和肿瘤促进细胞）。这些细胞彼此之间具有几种相互作用，这些相互作用主要通过细胞间介质的释放来调节。放射疗法可以通过将分泌物转变为炎症或抗炎反应来调节这些相互作用。放射疗法还可以通过激活基质细胞来触发癌细胞（干细胞）的耐药性。肿瘤对放射疗法的抗性的主要机制是通过抑制CD4 + T细胞和细胞毒性CD8 + T淋巴细胞（CTL）的凋亡来耗尽抗肿瘤免疫力。癌症相关的成纤维细胞（CAF），通过释放多种趋化因子，细胞因子和免疫抑制剂，间充质来源的抑制细胞（MDSCs）和调节性T细胞（Tregs）是主要的抗肿瘤免疫抑制剂。在这篇综述中，我们解释了放疗后TME中的主要细胞和分子相互作用以及分泌。此外，将讨论可用于提高放射治疗效率的主要信号通路和细胞间连接。