TABLE 1.
Immune cell lineage | Subtypes | Function | Metabolism |
---|---|---|---|
Macrophage | |||
M1 (classical activation) |
Pathogen clearance and antigen presentation Secretes pro‐inflammatory cytokines and express high levels of MHC |
Enhanced glycolysis, PPP, and FA synthesis | |
M2 (alternate activation) | Produce anti‐inflammatory cytokines to promote immunosuppression and tumor progression |
Increased OXPHOS and FAO decreased glycolysis and PPP |
|
Neutrophil |
Glycolysis If exposed to a TME deficient in glucose, adapt to mitochondrial FAO |
||
N1 (anti‐tumor) | Anti‐tumor polarization induced by type 1 IFNs | ||
N2 (pro‐tumor) | TGF‐β an overexpressed by tumor cells polarize neutrophils to pro‐tumor phenotype | ||
Neutrophil extracellular traps (NETs) | Fibers of decondensed DNA | Dependent on glucose and to a lesser extent on glutamine | |
NK cell | Critical in the early immune response regulating the adaptive immune response through the release of IFN‐γ |
Use OXPHOS during their resting state and upon short‐term activation Prolonged stimulation: switch to glycolysis |
|
T cell | |||
CD4+ Helper T cells | Mediator of immune function secreting cytokines to heighten immune response | Glycolysis and ACC‐mediated de novo FA synthesis | |
CD8+ Cytotoxic T cells | Direct cytotoxic killing of cancer cells | Enhanced glycolysis, glutaminolysis, and FAO to exert anti‐tumor cytotoxicity | |
Regulatory T cells | Dampen the immune response | FAO rather than glycolysis | |
Memory T cells | Protection against reinfection or tumor re‐emergence | Mitochondrial FAO for development and long‐term survival |