Metabolic reprogramming in macrophages and dendritic cells in innate immunity  

作　　者：Beth Kelly Luke AJ O'Neill 

机构地区：[1]School of Biochemistry and lmmunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Ireland

出　　处：《Cell Research》2015年第7期771-784,共14页细胞研究（英文版）

摘　　要：Activation of macrophages and dendritic cells （DCs） by pro-inflammatory stimuli causes them to undergo a metabolic switch towards glycolysis and away from oxidative phosphorylation （OXPHOS）, similar to the Warburg effect in tumors. However, it is only recently that the mechanisms responsible for this metabolic reprogramming have been elucidated in more detail. The transcription factor hypoxia-inducible factor-la （HIF-la） plays an important role un- der conditions of both hypoxia and normoxia. The withdrawal of citrate from the tricarboxylic acid （TCA） cycle has been shown to be critical for lipid biosynthesis in both macrophages and DCs. Interference with this process actually abolishes the ability of DCs to activate T cells. Another TCA cycle intermediate, succinate, activates HIF-la and pro- motes inflammatory gene expression. These new insights are providing us with a deeper understanding of the role of metabolic reprogramming in innate immunity.

关 键 词：MACROPHAGE dendritic cell metabolic reprogramming GLYCOLYSIS oxidative phosphorylation 

分 类 号：Q25[生物学—细胞生物学] Q26