Research Program for Receptor Biochemistry and Tumor Metabolism, Department of Pediatrics, University Hospital of the Paracelsus Medical University, Salzburg, Austria.
Department of Biosciences and Medical Biology, University of Salzburg, Salzburg, Austria.
Cancer Immunol Immunother. 2024 Nov 13;74(1):23. doi: 10.1007/s00262-024-03867-3.
Immune checkpoint blockade (ICB) is now part of the standard of care in the treatment of many forms of cancer, yet it lacks efficacy in some patients, necessitating adjunct therapies to support the anti-tumor immune response. Ketogenic diets (KDs), i.e., high-fat low-carbohydrate diets, have been shown to have antiproliferative and immunomodulatory effects in various preclinical cancer studies. Here, we review current knowledge of the complex interplay of KDs and the anti-tumor immune response in the context of ICB therapy, to update our understanding of diet-induced immunometabolic reprogramming in cancer. Preclinical cancer studies have revealed increased activation of and infiltration by tumor-fighting immune cells, especially CD8+ T cells, but also M1 macrophages and natural killer cells, in response to a KD regimen. In contrast, immune-suppressive cells such as regulatory CD4+ T lymphocytes, M2 macrophages, and myeloid-derived suppressor cells were reported to be decreased or largely unaffected in tumors of KD-fed mice. KDs also showed synergism with ICB therapy in several preclinical tumor studies. The observed effects are ascribed to the ability of KDs to improve immune cell infiltration and induce downregulation of immune-inhibitory processes, thus creating a more immunogenic tumor microenvironment. The studies reviewed herein show that altering the metabolic composition of the tumor microenvironment by a KD can boost the anti-tumor immune response and diminish even immunotherapy-resistant as well as immunologically "cold" tumors. However, the exact underlying mechanisms remain to be elucidated, requiring further studies before KDs can be successfully implemented as an adjunct tumor therapy to improve survival rates for cancer patients.
免疫检查点阻断 (ICB) 现已成为治疗多种癌症的标准治疗方法之一,但在某些患者中缺乏疗效,因此需要辅助治疗来支持抗肿瘤免疫反应。生酮饮食 (KDs),即高脂肪低碳水化合物饮食,已在各种临床前癌症研究中显示出具有抗增殖和免疫调节作用。在这里,我们回顾了 KDs 与 ICB 治疗中抗肿瘤免疫反应的复杂相互作用的现有知识,以更新我们对饮食诱导的癌症免疫代谢重编程的理解。临床前癌症研究表明,对 KD 方案的反应会增加肿瘤杀伤性免疫细胞的激活和浸润,特别是 CD8+ T 细胞,但也有 M1 巨噬细胞和自然杀伤细胞。相比之下,据报道,在 KD 喂养的小鼠肿瘤中,免疫抑制性细胞(如调节性 CD4+ T 淋巴细胞、M2 巨噬细胞和髓源性抑制细胞)减少或基本不受影响。KDs 还在几项临床前肿瘤研究中与 ICB 治疗表现出协同作用。观察到的这些作用归因于 KDs 改善免疫细胞浸润和诱导免疫抑制过程下调的能力,从而创造了更具免疫原性的肿瘤微环境。本文综述的研究表明,通过 KD 改变肿瘤微环境的代谢组成可以增强抗肿瘤免疫反应,并减少甚至免疫治疗耐药和免疫“冷”肿瘤。然而,确切的潜在机制仍有待阐明,需要进一步的研究,才能成功将 KDs 作为辅助肿瘤治疗方法实施,以提高癌症患者的生存率。