Abstract
Functional and effective immune response requires a metabolic rewiring of immune cells to meet their energetic and anabolic demands. Beyond this, the availability of extracellular and intracellular metabolites may serve as metabolic signals interconnecting with cellular signaling events to influence cellular fate and immunological function. As such, tumor microenvironment represents a dramatic example of metabolic derangement, where the highly metabolic demanding tumor cells may compromise the function of some immune cells by competing nutrients (a form of intercellular competition), meanwhile may support the function of other immune cells by forming a metabolic symbiosis (a form of intercellular collaboration). It has been well known that tumor cells harness immune system through information exchanges that are largely attributed to soluble protein factors and intercellular junctions. In this review, we will discuss recent advance on tumor metabolism and immune metabolism, as well as provide examples of metabolic communications between tumor cells and immune system, which may represent a novel mechanism of conveying tumor-immune privilege.
Highlights
The intercellular metabolic interplay between tumor and immune cellsThe metabolic reprograming in tumor contributes to its growth either by directly supporting cancer cell proliferation or by shaping the microenvironment potentially favoring tumor cell survival
Reviewed by: Christian Frezza, Hutchison/MRC Research Institute, UK Katiuscia Bianchi, Queen Mary University of London, UK
Tumor microenvironment represents a dramatic example of metabolic derangement, where the highly metabolic demanding tumor cells may compromise the function of some immune cells by competing nutrients, may support the function of other immune cells by forming a metabolic symbiosis
Summary
The metabolic reprograming in tumor contributes to its growth either by directly supporting cancer cell proliferation or by shaping the microenvironment potentially favoring tumor cell survival. Upon stimulation, activated T lymphocyte “reprograms” its metabolism, by dramatically increasing aerobic glycolysis and glutaminolysis decreasing lipid oxidation to meet its requirements for cell size growth, cell division, and cytokine production [35,36,37,38]. To mount a rapid inflammatory response, M1 macrophages coordinately engage aerobic glycolysis, pentose phosphate shunt (PPP), glutamine, and arginine catabolism to produce nitric oxide (NO) and reactive oxygen species (ROS) [58,59,60]. Metabolic regulation in NK and neutrophils are largely unknown
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