From: Reprogramming of lipid metabolism in the tumor microenvironment: a strategy for tumor immunotherapy
Immune cells | Indicators of lipid metabolism | Mechanisms | Diseases | References |
---|---|---|---|---|
TAM | FABP5 | Enhance FAO, oxidative phosphorylation and activate PPAR-γ signaling | Allergic airway inflammation | [20] |
FASN | Promote PPAR-δ activation and IL-10 release | Lung cancer | [21] | |
CD36 | Promote the uptake of LDs and LCFAs. Enhance the polarization of M2-TAMs | Liver metastases | [22] | |
PPAR | Promote FAO and the synthesis of M2-TAMs | HCC | [23] | |
25-hydroxycholesterol | Activate TLR4 and nuclear factor-κB signaling | Atherosclerosis | [83] | |
APOA1 ABCG1 | Promote cholesterol efflux | Atherosclerosis | [84] | |
Asprosin | Activate the p38/Elk-1 axis. Promote cholesterol efflux and inhibit lipid accumulation | Atherosclerosis | [84] | |
CD8 + T | CD36 | Promote uptake of FAs and FAO. Inhibit the release of IFN-γ, PRF1, GZMB, and TBX21 Promote uptake of oxLDL and P38 activation | - | |
very long-chain acyl-CoA dehydrogenase | Increases the very long-chain FA accumulation and FAO | PDAC | [39] | |
Cholesterol | Increasing ER stress and decrease GZMB, IFN-γ, and TNF-α levels | B16 and MC38 tumor models | [35] | |
LA | Enhance the formation of ER–mitochondrial contacts | - | [38] | |
SCFAs | Promote the production of CD25, IFN-γ and TNF-α | Pancreatic cancer model | [39] | |
Treg | CPT1A | Promote FAO and Treg differentiation | - | [42] |
CD36 | Activate the PPAR-β pathway and promote lipid uptake | - | [40] | |
FABP5 | increase OXPHOS and promote lipid metabolism | - | [45] | |
SREBP、FASN | inhibit FA synthesis and reduce cholesterol metabolism | - | [46] | |
DC cells | ACC | Increase the amount of DC lipids | - | [52] |
TDE、PPAR-α | Promote OXPHOS | B16/F10 melanoma model | [53] | |
CD36 | Increase lipid accumulation and phagocytosis by DCs | - | ||
FASN、LPA | Increased FA synthesis and lead to FA accumulation in DCs | Ovarian cancer | ||
Scavenging receptors | Promote lipid accumulation and decrease cytokine levels | HCC | [58] | |
CPT1A | Enhance FAO and promotes Treg development | Melanoma | [51] | |
LDs | Decrease the ability of DCs to activate T cells | Malignant mesothelioma | [59] | |
NK cells | lipid transporters and enzymes | Inhibit granase B and interferon production. Diminish NK effects | - | [62] |
MSR1 CD6 CD36 | lipid accumulation | Melanoma, breast, colorectal cancer | ||
lipids | Transfer lipids into NK-cell exosome-like vesicles and lead to NK cell dysfunction | Breast cancer and lung metastasis | [65] | |
Cholesterol SREBP2 | Induce FAO | - | [66] | |
long-chain acylcarnitine | Promote iNK T-cell senescence, cell cycle arrest, and telomere damage | HBV-associated HCC | [67] | |
MDSCs | ApoE | Promotes neutrophil senescence | Prostate tumor | [71] |
PMN-MDSCs | FATP2 | Increase lipid accumulation | Colon, pancreas, and lymphatic system cancers | |
XBP1 | Promotes cholesterol synthesis and secretion | - | [75] | |
CAFs | LPC | Create lysophosphatidic acid and accelerate tumor growth | PDAC | [79] |
FATP1 | Increase the intake of exogenous FAs | Triple-negative breast cancer | [60] | |
CD36 | promotes lipid peroxidation and p38 phosphorylation, | HCC | [80] |