Metabolic influence on the differentiation of suppressive myeloid cells in cancer

被引:26
作者
Porta, Chiara [1 ]
Marino, Arianna [1 ]
Consonni, Francesca Maria [2 ]
Bleve, Augusto [1 ]
Mola, Silvia [1 ]
Storto, Mariangela [1 ]
Riboldi, Elena [1 ]
Sica, Antonio [1 ,2 ]
机构
[1] Univ Piemonte Orientale Amedeo Avogadro, Dept Pharmaceut Sci, Novara, Italy
[2] Humanitas Clin & Res Ctr, Rozzano, Italy
关键词
TUMOR-ASSOCIATED MACROPHAGES; ARYL-HYDROCARBON RECEPTOR; FATTY-ACID OXIDATION; ANTITUMOR IMMUNITY; T-CELLS; INSULIN-RESISTANCE; OBESITY ALTERS; INFLAMMATION; ACTIVATION; PROMOTE;
D O I
10.1093/carcin/bgy088
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
New evidences indicate that the metabolic instruction of immunity (immune metabolism) results from the integration of cell metabolism and whole-body metabolism, which are both influenced by nutrition, microbiome metabolites and disease-driven metabolism (e.g. cancer metabolism). Cancer metabolism influences the immunological homeostasis and promotes immune alterations that support disease progression, hence influencing the clinical outcome. Cancer cells display increased glucose uptake and fermentation of glucose to lactate, even in the presence of completely functioning mitochondria. A major side effect of this event is immunosuppression, characterized by limited immunogenicity of cancer cells and restriction of the therapeutic efficacy of anticancer immunotherapy. Here, we discuss how the metabolism of myeloid cells associated with cancer contributes to the differentiation of their suppressive phenotype and therefore to cancer immune evasion.
引用
收藏
页码:1095 / 1104
页数:10
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