It induces persistent local inflammation (via IL-1β, IL-6, and TNF-α upregulation) and concurrently suppresses anti-tumor immunity: F. nucleatum adhesins (e.g., FadA and Fap2 proteins) allow it to bind colonocytes and immune cells, disrupting E-cadherin junctions and engaging T cell inhibitory receptors (like TIGIT) [77]. Here, IL1B is linked to neoplasm.