抗肿瘤药物的使用代表了癌症治疗的可靠策略。不幸的是，耐药性变得越来越普遍，并导致肿瘤转移和局部复发。肿瘤免疫微环境（TME）由免疫细胞、细胞因子和免疫调节剂组成，它们共同影响对治疗的反应。据报道，包括 DNA 甲基化和组蛋白修饰在内的表观遗传变化以及药物输出的增加有助于癌症耐药性的发展。过去几年，大多数关于肿瘤的研究都只是从机制的角度来研究肿瘤的发生、发展过程，而对于肿瘤的研究则主要集中在肿瘤的发生、发展过程中。很少有研究探讨 TME 的变化是否也会影响肿瘤生长和耐药性。最近，新出现的证据引起了人们对 TME 在耐药性发展中的作用的更多关注。在本综述中，讨论了抑制性 TME 如何适应以免疫细胞、细胞因子、免疫调节剂、基质细胞和细胞外基质合作为特征的耐药性。此外，还回顾了这些免疫或代谢变化如何改变免疫监视，从而促进肿瘤耐药性。此外，还揭示了 TME 中存在的潜在目标，用于开发新的治疗策略，以改善癌症治疗的个体化治疗。

The use of antitumor drugs represents a reliable strategy for cancer therapy. Unfortunately, drug resistance has become increasingly common and contributes to tumor metastasis and local recurrence. The tumor immune microenvironment (TME) consists of immune cells, cytokines and immunomodulators, and collectively they influence the response to treatment. Epigenetic changes including DNA methylation and histone modification, as well as increased drug exportation have been reported to contribute to the development of drug resistance in cancers. In the past few years, the majority of studies on tumors have only focused on the development and progression of a tumor from a mechanistic standpoint; few studies have examined whether the changes in the TME can also affect tumor growth and drug resistance. Recently, emerging evidence have raised more concerns regarding the role of TME in the development of drug resistance. In the present review, it was discussed how the suppressive TME adapts to drug resistance characterized by the cooperation of immune cells, cytokines, immunomodulators, stromal cells and extracellular matrix. Furthermore, it was reviewed how these immunological or metabolic changes alter immuno‑surveillance and thus facilitate tumor drug resistance. In addition, potential targets present in the TME for developing novel therapeutic strategies to improve individualized therapy for cancer treatment were revealed.