Chronic inflammation promotes tumor development, progression, and metastatic dissemination and causes treatment resistance. The accumulation of genetic alterations and loss of normal cellular regulatory processes are not only associated with cancer growth and progression but also result in the expression of tumor-specific and tumor-associated antigens that may activate antitumor immunity. This antagonism between inflammation and immunity and the ability of cancer cells to avoid immune detection affect the course of cancer development and treatment outcomes. While inflammation, particularly acute inflammation, supports T-cell priming, activation, and infiltration into infected tissues, chronic inflammation is mostly immunosuppressive. However, the main mechanisms that dictate the outcome of the inflammation-immunity interplay are not well understood. Recent data suggest that inflammation triggers epigenetic alterations in cancer cells and components of the tumor microenvironment. These alterations can affect and modulate numerous aspects of cancer development, including tumor growth, the metabolic state, metastatic spread, immune escape, and immunosuppressive or immunosupportive leukocyte generation. In this review, we discuss the role of inflammation in initiating epigenetic alterations in immune cells, cancer-associated fibroblasts, and cancer cells and suggest how and when epigenetic interventions can be combined with immunotherapies to improve therapeutic outcomes.

慢性炎症促进肿瘤的发生、进展和转移扩散，并导致治疗抵抗。基因改变的积累和正常细胞调节过程的丧失不仅与癌症的生长和进展有关，而且还导致肿瘤特异性和肿瘤相关抗原的表达，从而可能激活抗肿瘤免疫。炎症和免疫之间的这种对抗以及癌细胞逃避免疫检测的能力会影响癌症的发展过程和治疗结果。虽然炎症，特别是急性炎症，支持 T 细胞启动、激活和渗透到受感染的组织中，但慢性炎症主要是免疫抑制的。然而，决定炎症-免疫相互作用结果的主要机制尚不清楚。最近的数据表明，炎症会引发癌细胞和肿瘤微环境成分的表观遗传改变。这些改变可以影响和调节癌症发展的许多方面，包括肿瘤生长、代谢状态、转移扩散、免疫逃逸以及免疫抑制或免疫支持性白细胞生成。在这篇综述中，我们讨论了炎症在免疫细胞、癌症相关成纤维细胞和癌细胞中引发表观遗传改变的作用，并建议如何以及何时将表观遗传干预与免疫疗法相结合以改善治疗结果。