Table 1.

Impact of lipid metabolism and signalling on the tumour immune microenvironment.

Cell types	Lipid abnormality	Impact on cell differentiation and function	Impact on anti-tumour response
CD8+T cells	Increased lipid uptake and FAO; triggering the LPC-ATX-LPA axis, PPAR, and tumour-derived PGE2 signalling	Inhibition or enhancement of effector function depending on condition	Unsure
Tregs	Increased lipid biosynthesis and FAO; upregulation of CD36; triggering the PPAR signalling	Obtaining metabolic adaptations and advantages to survive and proliferate	Immunosuppressive effects
Macrophages	Lipid accumulation and increased FAO; cholesterol efflux	Polarisation to an M2 phenotype	Immunosuppressive effects
Neutrophils	Increased FAO	Maintaining ROS production and T cell suppression	Immunosuppressive effects
MDSC	Upregulation of FATP2; increased uptake of arachidonic acid and synthesis of PGE2; increased FAO; triggering tumour-derived PGE2 signalling	Promoting T cell suppression by MDSC	Immunosuppressive effects
DC	Increased LD accumulation and FAO; triggering tumour-derived PGE2 signalling	Limiting the recruitment of DCs and leading to dysfunction	Immunosuppressive effects
NK	Increased uptake and accumulation of exogenous lipids; triggering tumour-derived PGE2 signalling	Impairing cell viability and blunt function	Immunosuppressive effects

ATX, autotaxin; DCs, dendritic cells; FAO, fatty acid oxidation; FATP2, fatty acid transport protein 2; LDs, lipid droplets; LPA, lysophosphatidic acid; LPC, lysophosphatidylcholine; MDSC, myeloid-derived suppressor cells; NK, natural killer; PGE2: prostaglandin-E2; PPAR, peroxisome proliferator-activated receptors; ROS, reactive oxygen species; Tregs, immune regulatory T cells.