肿瘤细胞治疗研究
英文原题：Nicotinamide mononucleotide enhances anti-tumor effect by resetting macrophages toward the inflammatory M1-like phenotype.
补充烟酰胺单核苷酸（NMN）已通过调控能量产生过程中的代谢活动显示出临床获益。
烟酰胺单核苷酸（NMN）补充剂可通过调节能量生成过程中的代谢活动带来临床获益。然而，其对肿瘤进展的保护作用及相关免疫调节机制仍知之甚少。我们发现，高剂量NMN处理可改变人免疫细胞中若干关键NAD+代谢酶的水平。此外，在小鼠间皮瘤挑战模型中，高剂量NMN处理显示出与PD-1阻断相当的抗肿瘤疗效。对继发淋巴器官和肿瘤的后续免疫分析发现，与调节T细胞和NK细胞应答不同，高剂量NMN处理可使肿瘤相关巨噬细胞转变为炎症性M1样表型，且与PD-1阻断组或未处理组相比均如此。这些结果加深了对NMN调节免疫细胞作用的理解，并提示其可能成为癌症免疫治疗的替代策略。
Nicotinamide mononucleotide (NMN) supplementation has shown clinical benefits by regulating metabolic activities in the energy production process. Its protective effect and underlying immune regulatory mechanisms against tumor progression are still poorly understood. Here, we found that the high-dose NMN treatment could alter the level of several key NAD + metabolic enzymes in human immune cells. Moreover, high-dose NMN treatment exhibited comparable antitumor efficacy as the PD-1 blockade in the murine mesothelioma challenge model. Subsequent immune profiling in both secondary lymphoid organ and tumor demonstrated that, rather than modulating T cell and NK cell responses, high-dose NMN treatment could reset tumor-associated macrophages toward the inflammatory M1-like phenotype compared with PD-1 blockade or non-treated subjects. These results provided a better understanding of NMN's regulatory effect on immune cells and suggested an alternative strategy of cancer immunotherapy.
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