Fig. 2

Lipid metabolism in anti-tumor immune response. a Trms take in FAs from the TME via CD36 and FATPs to generate anti-tumor cytokines like GzmB, IFN-γ, and TNF-α. Moreover, cholesterol helps the formation of TCRs on Teffs and stimulates their proliferation and cytotoxicity. PPAR-α/γ also enhances the anti-tumor ability of Teffs through activating FAO; b FAs in the TME enhance FAO in macrophages, which upregulate ROS production, downregulate IL-10 secretion, and eliminate tumor cells. Elevated E-FABPs in macrophages promote IFN-β expression and mediates the recruitment of NK cells to kill tumor cells; c Cholesterol taken in via LDLR stimulates the expression of effector markers (GzmB and perforin), cytokines, and chemokines. Activated PPAR-γ in NK cells promotes the secretion of IFN-γ, which is suppressed by excessive lactic acid in the TME; d triglyceride and phospholipid enhance the cross-presentation ability and cytokine secretion level of DCs to participate in the anti-tumor response