Fig.1

Biological roles of the glycolysis and cholesterol metabolism axis in T cells and DCs-relevant TME. For figure: important glycolysis and cholesterol metabolic crosstalk onto which cells rely are shown in colour; less critical or studied pathways are shown in outside. The glycolysis and cholesterol interconnections exert transinhibition of metabolic signaling in TME-relevant T cells and DCs, and indirectly control neutrophils and Tregs. Scheme of the glycolysis and cholesterol metabolic axis in antitumor immune milieu in response to harsh TME are presented. These factors can perturb proliferation, maturation, activation, migration, or co-stimulatory molecule signaling in T cells and/or DCs. i Distant and proximal roles between glycolysis and cholesterol metabolic axis in the TME (Red). Only the undefined or indirect association was marked by dashed lines. ii Glycolysis dominant intracellular metabolic signaling to secure energy requirements (Blue). iii Cholesterol dominant inner or outer signal transduction and cellular functions (Green). However, several important mechanisms of cholesterol to T cells or IL-10-related DCs metabolism are unclear (denoted by question marks). Each arrow line represented the relationship directly bridge between each other. Glu: Glucose; ER stress: Endoplasmic reticulum stress; TME: Tumor microenvironment; TCR: T-cell receptor; ACAT1: Acetyl-CoA acetyltransferase 1; NKTs: nature killer T cells; LDLR: Low-density lipoprotein receptor; TCA: Tricarboxylic acid cycle; ATP: Adenosine-triphosphate; LXR: Liver X receptors; OXPHOS: Oxidative phosphorylation