IL17A and neoplasm: Fusobacterium nucleatum binds CRC cells via FadA, inducing IL-6, IL-8, and IL-18, while Escherichia coli virulence factor CNF1 triggers IL-6 and TNF-α, sustaining chronic inflammation that promotes tumor progression.[6] Intratumoral bacteria also stimulate myeloid cells to produce MyD88-dependent IL-1β and IL-23, activating γδT cells to secrete IL-17, which promotes B cell infiltration and tumor progression.