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. 2023 Feb 23;24(5):4422. doi: 10.3390/ijms24054422

Figure 1.

Figure 1

Interactions between tumor endothelial cells (ECs) and immune populations to create the tumor immune microenvironment. Tumor blood vessel abnormalities results from an imbalance between pro- and anti-angiogenic signaling, which in turn results in a hypoxic and acidic TME. The hypoxia and acidosis regulate the immune response through pro-tumoral and anti-tumoral arms. The activation of endothelial cells can facilitate or inhibit tumor immunity through multiple pathways, including contact-dependent and soluble factor-mediated pathways. The blue arrows depict upregulation. The red lines show suppressive effects. MCT: Monocarboxylate transporter; HIF: Hypoxia-inducible factor; TAM: Tumor-associated macrophage; Treg: regulatory T cell; NK: natural killer; Ang-2: Angiopoietin 2; PSGL1: P-selectin glycoprotein ligand-1; VEGF: Vascular endothelial growth factor; VCAM: vascular cell adhesion protein; ICAM: Intercellular adhesion molecule; STAT3: Signal transducer and activator of transcription 3; NF-κB: Nuclear factor kappa-B; TCR: T cell receptor; HEVs: High endothelial venules; IFN-γ: Interferon-γ.