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Journal of Immunology Research
Volume 2018, Article ID 8605471, 12 pages
https://doi.org/10.1155/2018/8605471
Review Article

Regulation of Immune Cell Functions by Metabolic Reprogramming

1Department of Biochemistry, School of Medicine, Gachon University, Incheon 21999, Republic of Korea
2Department of Health Sciences and Technology, Gachon Advanced Institute for Health Science and Technology, Gachon University, Incheon 21999, Republic of Korea

Correspondence should be addressed to Jaehong Kim; rk.ca.nohcag@scitereg

Received 19 October 2017; Accepted 14 January 2018; Published 13 February 2018

Academic Editor: Abdallah Elkhal

Copyright © 2018 Jaehong Kim. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Recent findings show that the metabolic status of immune cells can determine immune responses. Metabolic reprogramming between aerobic glycolysis and oxidative phosphorylation, previously speculated as exclusively observable in cancer cells, exists in various types of immune and stromal cells in many different pathological conditions other than cancer. The microenvironments of cancer, obese adipose, and wound-repairing tissues share common features of inflammatory reactions. In addition, the metabolic changes in macrophages and T cells are now regarded as crucial for the functional plasticity of the immune cells and responsible for the progression and regression of many pathological processes, notably cancer. It is possible that metabolic changes in the microenvironment induced by other cellular components are responsible for the functional plasticity of immune cells. This review explores the molecular mechanisms responsible for metabolic reprogramming in macrophages and T cells and also provides a summary of recent updates with regard to the functional modulation of the immune cells by metabolic changes in the microenvironment, notably the tumor microenvironment.