Cancer cells are often described as voracious consumers of nutrients, with glucose frequently cited as a key energy source; however, their metabolic plasticity allows them to adapt and utilize various substrates, including lipids and amino acids, to sustain growth and survival. However, the metabolic demands of immune cells within the tumor microenvironment (TME) are less commonly discussed despite their critical role in shaping the immune response. In this review, we explored the intricate interplay between immunometabolism and innate immunity cells in gastrointestinal cancers. We focused on how metabolic pathways, including glycolysis, fatty acid oxidation, and amino acid metabolism, drive the immunosuppressive functions of myeloid-derived suppressor cells (MDSCs) and tumor-associated neutrophils (TANs), tumor-associated macrophages (TAMs) and innate lymphocyte subsets such as NK cells. These cells contribute to a hostile immune landscape, supporting tumor growth and evasion from immune surveillance in a phenomenon of tumor-derived immunosuppression. Additionally, we investigated the influence of dietary interventions on the metabolic reprogramming of these immune cells, highlighting how nutrition can modulate the TME. Finally, we discussed emerging therapeutic strategies that target metabolic vulnerabilities in MDSCs, TANs, NK cells, and monocytes, offering a novel avenue for enhancing antitumor immunity. By dissecting these mechanisms, we aim to provide insights into how metabolic pathways can be harnessed to improve cancer treatment outcomes. This review underscores the importance of understanding immunometabolism not only as a driver of immune suppression but also as a potential therapeutic target in gastrointestinal cancer.
癌细胞常被描述为营养物质的贪婪消耗者，葡萄糖常被视为关键能量来源；然而，其代谢可塑性使其能够适应并利用多种底物（包括脂质和氨基酸）以维持生长和存活。尽管肿瘤微环境（TME）中免疫细胞的代谢需求在塑造免疫反应中具有关键作用，却较少被讨论。本综述探讨了胃肠道癌症中免疫代谢与先天免疫细胞之间复杂的相互作用。我们重点关注糖酵解、脂肪酸氧化和氨基酸代谢等代谢途径如何驱动髓源性抑制细胞（MDSCs）、肿瘤相关中性粒细胞（TANs）、肿瘤相关巨噬细胞（TAMs）以及自然杀伤细胞（NK细胞）等先天淋巴细胞亚群的免疫抑制功能。这些细胞共同构成了抑制性的免疫微环境，通过肿瘤源性免疫抑制现象支持肿瘤生长并逃避免疫监视。此外，我们研究了饮食干预对这些免疫细胞代谢重编程的影响，揭示了营养如何调控肿瘤微环境。最后，我们讨论了针对MDSCs、TANs、NK细胞和单核细胞代谢脆弱性的新兴治疗策略，为增强抗肿瘤免疫提供了新途径。通过解析这些机制，我们旨在揭示如何利用代谢途径改善癌症治疗效果。本综述强调，理解免疫代谢不仅作为免疫抑制的驱动因素，更应被视为胃肠道癌症的潜在治疗靶点。
Immunometabolism of Innate Immune Cells in Gastrointestinal Cancer
肿瘤(癌症)患者之家