Core Viewpoint - Dietary restriction (DR) can extend the lifespan of mammals and delay age-related diseases, including cancer, through mechanisms that are not yet fully understood [1]. Group 1: Research Findings - A study published in Nature Metabolism indicates that dietary restriction leads to metabolic changes in ketone bodies, specifically increasing β-hydroxybutyrate (βOHB), which reprograms the fate and function of CD8+ T cells in the tumor microenvironment, enhancing anti-tumor immunity and responses to immunotherapy [1]. - In experiments, mice subjected to a 50% dietary restriction showed a significant slowdown in tumor growth and a survival extension of 30%-80% compared to those with free access to food [4]. - The anti-cancer effects of dietary restriction were found to be dependent on the immune system, particularly CD8+ T cells, as the effects disappeared in T cell-deficient mice [4]. Group 2: Mechanism of Action - CD8+ T cells, known as "killer cells," are responsible for identifying and destroying cancer cells, but often become "exhausted" in the tumor microenvironment [6]. - Dietary restriction promotes the expansion of effector T cell subsets with stronger anti-cancer capabilities while limiting the accumulation of terminally exhausted T cells [7]. - The mechanism behind this transformation is linked to ketone metabolism, where increased βOHB enhances mitochondrial function and energy metabolism in CD8+ T cells, thereby boosting their anti-cancer capabilities [8]. Group 3: Implications for Cancer Therapy - The study found that dietary restriction can synergize with existing cancer immunotherapies, such as PD-1 monoclonal antibodies, significantly improving treatment outcomes and even leading to complete tumor regression in some melanoma mouse models [9]. - The research suggests that dietary interventions could be a simple and effective strategy to enhance the efficacy of cancer immunotherapy [11]. - Given the challenges of implementing strict dietary restrictions in clinical settings, alternative approaches such as GLP-1 receptor agonists (e.g., semaglutide, tirzepatide) may simulate the metabolic effects of dietary restriction [11].