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| TIGIT (T Cell Immunoreceptor With Ig And ITIM Domains) — Inhibitory immune-checkpoint receptor expressed primarily on activated T cells, exhausted T cells, regulatory T cells, and natural killer (NK) cells. TIGIT binds mainly to CD155/PVR and also to CD112/NECTIN2, suppressing T-cell and NK-cell activation and cytotoxicity. Typical modulation in cancer: Frequently ↑ on tumor-infiltrating lymphocytes and generally unfavorable. Increased TIGIT signaling is associated with T-cell exhaustion, reduced NK-cell cytotoxicity, immune evasion, and impaired antitumor immunity. TIGIT blockade is being investigated clinically, often in combination with PD-1/PD-L1 inhibition. Typical mechanistic relationship: CD155/PVR or CD112/NECTIN2 → TIGIT activation → inhibitory signaling ↑ → T-cell activation ↓, NK-cell cytotoxicity ↓, cytokine production ↓, and tumor immune escape ↑. Competitive signaling: CD155/PVR can also bind the activating receptor CD226/DNAM-1. TIGIT competes with CD226 for ligand binding and generally shifts signaling toward immune inhibition. |
| 9246- | ISO, IH, | Isorhamnetin inhibits migration and promotes apoptosis via modulation of oxidative stress, mitochondrial dysfunction, and the TIGIT/CD155 axis in 4T1 breast cancer cells |
| - | in-vitro, | BC, | 4T1 |
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