炎症是机体的免疫细胞在损伤和抗损伤过程中重要的病理生理事件。在病原微生物如细菌、病毒等侵入机体时，机体被感染的免疫细胞常会分泌大量炎性细胞因子进行抗感染免疫应答，如干扰素等。而髓系抑制细胞（myeloid-derived suppressor cells, MDSCs）由于常显示免疫抑制作用，在促肿瘤和抑感染中等有重要意义。因此，如何靶向髓系抑制细胞，有效干预其抑制活性，就成为防治肿瘤和感染的有效途径。如何靶向髓系抑制细胞的代谢信号进行调控其发育和功能，一直是该领域的研究热点。本文采用多种细胞生物学和免疫学方法，研究了炎症微环境依赖烟酰胺腺嘌呤二核苷酸（NAD）补救途径干预糖酵解信号从而调控髓系抑制细胞的体外诱导分化过程。该结果将为靶向髓系抑制细胞的细胞代谢信号调控免疫相关疾病的研究提供实验依据。

Inflammation is an important pathophysiological event of the body's immune cells in the process of injury and anti-injury. When pathogenic microorganisms such as bacteria and viruses invade the body, the infected immune cells often secrete a large number of inflammatory cytokines, such as interferons, to carry out an anti-infection immune response. Myeloid-derived suppressor cells (MDSCs) are reported to exert immunosuppressive effects, and are of great significance in promoting tumors and suppressing infections, hence how to target myeloid-derived suppressor cells and effectively intervene their inhibitory activity has become an effective way to prevent tumors and infections. Furthermore, how to target the metabolic signals of myeloid-derived suppressor cells to regulate their development and function has been a research highlight in related field. In this thesis, a variety of cell biology and immunological methods are used to clarify the inflammatory microenvironment dependent nicotinamide adenine dinucleotide (NAD) salvage pathway to intervene in glycolytic signals to regulate the in vitro differentiation process of myeloid-derived suppressor cells. The results will provide experimental basis for the research on the regulation of immune-related diseases by the cellular metabolism signal of targeting myeloid-derived suppressor cells.