Nutritional effects on T-cell immunometabolism

被引:128
作者
Cohen, Sivan [1 ]
Danzaki, Keiko [2 ]
MacIver, Nancie J. [1 ,2 ,3 ]
机构
[1] Duke Univ, Sch Med, Dept Pharmacol & Canc Biol, Durham, NC USA
[2] Duke Univ, Sch Med, Dept Pediat, Durham, NC USA
[3] Duke Univ, Sch Med, Dept Immunol, Durham, NC USA
基金
美国国家卫生研究院;
关键词
Glucose metabolism; Leptin; Malnutrition; Obesity; T cells; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; CONGENITAL LEPTIN DEFICIENCY; ADIPOSE-TISSUE INFLAMMATION; DIET-INDUCED OBESITY; HIGH-FAT DIET; INSULIN-RESISTANCE; LYMPHOCYTE-ACTIVATION; MEDIATED-IMMUNITY; MALNOURISHED CHILDREN;
D O I
10.1002/eji.201646423
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
T cells are highly influenced by nutrient uptake from their environment, and changes in overall nutritional status, such as malnutrition or obesity, can result in altered T-cell metabolism and behavior. In states of severe malnutrition or starvation, T-cell survival, proliferation, and inflammatory cytokine production are all decreased, as is T-cell glucose uptake and metabolism. The altered T-cell function and metabolism seen in malnutrition is associated with altered adipokine levels, most particularly decreased leptin. Circulating leptin levels are low in malnutrition, and leptin has been shown to be a key link between nutrition and immunity. The current view is that leptin signaling is required to upregulate activated T-cell glucose metabolism and thereby fuel T-cell activation. In the setting of obesity, T cells have been found to have a key role in promoting the recruitment of inflammatory macrophages to adipose depots along with the production of inflammatory cytokines that promote the development of insulin resistance leading to diabetes. Deletion of T cells, key T-cell transcription factors, or pro-inflammatory T-cell cytokines prevents insulin resistance in obesity and underscores the importance of T cells in obesity-associated inflammation and metabolic disease. Altogether, T cells have a critical role in nutritional immunometabolism.
引用
收藏
页码:225 / 235
页数:11
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