免疫检查点抑制改变了晚期黑色素瘤的治疗格局，患者的长期生存现在成为可能。然而，至少一半的患者没有充分受益。代谢重编程是癌细胞的标志，可能有助于肿瘤生长和肿瘤的免疫逃避。临床前研究确实证明，调节肿瘤代谢可以减少肿瘤生长，同时改善免疫细胞的功能。由于代谢途径通常在免疫细胞和肿瘤细胞之间共享，因此有必要了解调节患者的肿瘤代谢如何影响肿瘤微环境中促肿瘤和抗肿瘤免疫作用的复杂平衡。关键问题是调节肿瘤代谢是否可以抑制肿瘤细胞生长并促进抗肿瘤免疫反应。在这里，我们回顾了目前关于肿瘤代谢对黑色素瘤免疫反应影响的知识。我们总结了肿瘤微环境中黑色素瘤和非癌细胞的代谢途径，并讨论了可用于研究代谢-免疫相互作用的模型和技术。最后，我们讨论这些技术的临床应用，以提高我们对代谢干预如何使黑色素瘤患者的平衡向有利的、免疫许可的微环境倾斜的理解。版权所有 © 2024 作者。由爱思唯尔有限公司出版。保留所有权利。

Immune checkpoint inhibition has transformed the treatment landscape of advanced melanoma and long-term survival of patients is now possible. However, at least half of the patients do not benefit sufficiently. Metabolic reprogramming is a hallmark of cancer cells and may contribute to both tumour growth and immune evasion by the tumour. Preclinical studies have indeed demonstrated that modulating tumour metabolism can reduce tumour growth while improving the functionality of immune cells. Since metabolic pathways are commonly shared between immune and tumour cells, it is essential to understand how modulating tumour metabolism in patients influences the intricate balance of pro-and anti-tumour immune effects in the tumour microenvironment. The key question is whether modulating tumour metabolism can inhibit tumour cell growth as well as facilitate an anti-tumour immune response. Here, we review current knowledge on the effect of tumour metabolism on the immune response in melanoma. We summarise metabolic pathways in melanoma and non-cancerous cells in the tumour microenvironment and discuss models and techniques available to study the metabolic-immune interaction. Finally, we discuss clinical use of these techniques to improve our understanding of how metabolic interventions can tip the balance towards a favourable, immune permissive microenvironment in melanoma patients.Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.