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SCFAs (C2-C4) can potentiate CD8 T-cell metabolism and dendritic-cell competence, enhancing antiPD-1 responses in defined settings [90,91,92], yet systemic SCFAs can blunt CTLA-4 blockade, curb NK-cell effector function, or favor myeloid immunosuppression via FFAR2 MDSCs [53, 89, 103]
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As the dominant G-actin sequestering protein in mammalian cells, TB-500 binds globular actin with high affinity (Kd ~0.5 M) through a sophisticated triple-contact mechanism involving Lys-3, Lys-18, and Lys-38 residues, preventing spontaneous actin polymerization while maintaining a readily mobilizable reservoir for rapid cytoskeletal reorganization
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