Mechanical barriers: physical impediments to a direct contact between T cells and cancer cells |
|
ECM remodeling |
Cancer-associated fibrosis |
(42–48) |
Epithelial-to mesenchymal transition |
(49–55) |
Filaggrin, desmosomal proteins, endothelin B receptor |
(30, 56–58) |
Vascular accessibility |
HIF-1 and HIF-2 driven angiogenesis |
(59–63) |
Cancer cell coating |
CXCL12 |
(64–66) |
Functional barriers: determinants limiting migration, function, and/or survival of T cells |
|
Metabolic alterations TME |
Decrease in amino acids in the TME |
(67–72) |
Warburg effect (increase in lactate) |
(73–76) |
Increase in extracellular adenosine |
(77–80) |
Increase in potassium |
(62, 81, 82) |
Altered lipid metabolism |
(83) |
Cyclooxygenase and prostaglandin metabolism |
(84–86) |
Hypoxia |
(87–91) |
Soluble factors |
VEGF-α |
(59, 60, 92–94) |
Cytokines mediated immune suppressive mechanisms |
(42, 43, 95–98) |
Danger sensing molecules |
TAM receptors |
(99–102) |
don’t eat me signals |
(103–105) |
Tolerogenic cell death/absent immunogenic cell death |
(106–108) |
Tumor cell signaling |
STAT-3, PI3K, NF-κB, Wnt/β-catenin, MAPK, p53 |
(109–114) |
Dynamic barriers: barriers arising after interaction between T cells and cancer cells |
|
|
Checkpoint/ligand interactions |
(39–41) |