与正常组织相比，腺苷 (Ado) 在肿瘤微环境 (TME) 中显着升高。它与腺苷受体（AdoR）结合，抑制肿瘤抗原呈递和免疫细胞激活，从而抑制肿瘤适应性免疫。 Ado 下调主要组织相容性复合体 II (MHC II) 以及树突状细胞 (DC) 和巨噬细胞上的共刺激因子，从而抑制抗原呈递。它通过破坏 T 细胞受体 (TCR) 结合和信号转导来抑制抗肿瘤细胞因子的分泌和 T 细胞活化。 Ado 还抑制趋化因子分泌和 KCa3.1 通道活性，阻止效应 T 细胞运输和浸润到肿瘤部位。此外，Ado 通过促进免疫抑制细胞因子的分泌、上调免疫检查点蛋白和增强免疫抑制细胞活性来减少 T 细胞对肿瘤细胞的细胞毒性。减少TME中Ado的产生可以显着增强抗肿瘤免疫反应并提高其他免疫疗法的疗效。针对 Ado 生成或 AdoR 的抑制剂的临床前和临床开发正在进行中。因此，本文将总结分析Ado对肿瘤适应性免疫的抑制作用和分子机制，并概述靶向Ado通路在抗肿瘤免疫反应中的最新进展。© 2024 The Authors.

Adenosine (Ado) is significantly elevated in the tumor microenvironment (TME) compared to normal tissues. It binds to adenosine receptors (AdoRs), suppressing tumor antigen presentation and immune cell activation, thereby inhibiting tumor adaptive immunity. Ado downregulates major histocompatibility complex II (MHC II) and co-stimulatory factors on dendritic cells (DCs) and macrophages, inhibiting antigen presentation. It suppresses anti-tumor cytokine secretion and T cell activation by disrupting T cell receptor (TCR) binding and signal transduction. Ado also inhibits chemokine secretion and KCa3.1 channel activity, impeding effector T cell trafficking and infiltration into the tumor site. Furthermore, Ado diminishes T cell cytotoxicity against tumor cells by promoting immune-suppressive cytokine secretion, upregulating immune checkpoint proteins, and enhancing immune-suppressive cell activity. Reducing Ado production in the TME can significantly enhance anti-tumor immune responses and improve the efficacy of other immunotherapies. Preclinical and clinical development of inhibitors targeting Ado generation or AdoRs is underway. Therefore, this article will summarize and analyze the inhibitory effects and molecular mechanisms of Ado on tumor adaptive immunity, as well as provide an overview of the latest advancements in targeting Ado pathways in anti-tumor immune responses.© 2024 The Authors.