CD4+和CD8+T淋巴细胞是医治肿瘤的适应性免疫反应的主要介质。特定于肿瘤抗原的幼稚T淋巴细胞由树突状细胞在淋巴结中获得激活。一旦激活，抗原特异性T细胞会增殖并分化为效应细胞，以试图消除癌细胞并移动至肿瘤部位。完成功能后，大部分效应T细胞会在组织中死亡，而少量特异性T细胞会持续作为长寿命的记忆细胞在外周血液和淋巴组织之间循环，以增强在再次遇到相同抗原时的免疫反应。一部分记忆T细胞，称为长驻留记忆T细胞（TRM）细胞，稳定地驻留在非淋巴静脉组织中并可能独立于从血液中招募的T细胞提供迅速免疫力。由于适应于组织微环境，TRM细胞潜在地具有对抗肿瘤细胞再次出现的最佳特征。然而，当肿瘤出现临床表现时，这意味着肿瘤细胞已躲避了免疫监视，包括TRM细胞的监视。在这里，我们回顾了有关TRM细胞在免疫应答期间如何产生并在非淋巴组织中保持的当前知识。然后我们关注CD4+和CD8+TRM细胞在抗肿瘤免疫力中的角色及其可能对免疫疗法疗效的贡献。最后，我们强调该领域存在的一些未决问题，并讨论新技术如何帮助解决这些问题。© 2022年。作者（们）。

CD4+ and CD8+ T lymphocytes mediate most of the adaptive immune response against tumors. Naïve T lymphocytes specific for tumor antigens are primed in lymph nodes by dendritic cells. Upon activation, antigen-specific T cells proliferate and differentiate into effector cells that migrate out of peripheral blood into tumor sites in an attempt to eliminate cancer cells. After accomplishing their function, most effector T cells die in the tissue, while a small fraction of antigen-specific T cells persist as long-lived memory cells, circulating between peripheral blood and lymphoid tissues, to generate enhanced immune responses when re-encountering the same antigen. A subset of memory T cells, called resident memory T (TRM) cells, stably resides in non-lymphoid peripheral tissues and may provide rapid immunity independently of T cells recruited from blood. Being adapted to the tissue microenvironment, TRM cells are potentially endowed with the best features to protect against the reemergence of cancer cells. However, when tumors give clinical manifestation, it means that tumor cells have evaded immune surveillance, including that of TRM cells. Here, we review the current knowledge as to how TRM cells are generated during an immune response and then maintained in non-lymphoid tissues. We then focus on what is known about the role of CD4+ and CD8+ TRM cells in antitumor immunity and their possible contribution to the efficacy of immunotherapy. Finally, we highlight some open questions in the field and discuss how new technologies may help in addressing them.© 2022. The Author(s).