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Exploring the Potential of Glycolytic Modulation in Myeloid-Derived Suppressor Cells for Immunotherapy and Disease Management.
Kim, Jisu; Choi, Jee Yeon; Min, Hyeyoung; Hwang, Kwang Woo.
Afiliação
  • Kim J; College of Pharmacy, Chung-Ang University, Seoul 06974, Korea.
  • Choi JY; College of Pharmacy, Chung-Ang University, Seoul 06974, Korea.
  • Min H; College of Pharmacy, Chung-Ang University, Seoul 06974, Korea.
  • Hwang KW; College of Pharmacy, Chung-Ang University, Seoul 06974, Korea.
Immune Netw ; 24(3): e26, 2024 Jun.
Article em En | MEDLINE | ID: mdl-38974210
ABSTRACT
Recent advancements in various technologies have shed light on the critical role of metabolism in immune cells, paving the way for innovative disease treatment strategies through immunometabolism modulation. This review emphasizes the glucose metabolism of myeloid-derived suppressor cells (MDSCs), an emerging pivotal immunosuppressive factor especially within the tumor microenvironment. MDSCs, an immature and heterogeneous myeloid cell population, act as a double-edged sword by exacerbating tumors or mitigating inflammatory diseases through their immune-suppressive functions. Numerous recent studies have centered on glycolysis of MDSC, investigating the regulation of altered glycolytic pathways to manage diseases. However, the specific changes in MDSC glycolysis and their exact functions continue to be areas of ongoing discussion yet. In this paper, we review a range of current findings, including the latest research on the alteration of glycolysis in MDSCs, the consequential functional alterations in these cells, and the outcomes of attempts to modulate MDSC functions by regulating glycolysis. Ultimately, we will provide insights into whether these research efforts could be translated into clinical applications.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article