IL17A and colitis: Through transcriptomic profiling of 192 clinical strains, Kovács et al. identified oxidative stress resistance, biofilm formation, and metabolic adaptation as key survival strategies.253 In IL-10−/− mice, C. jejuni infection induced severe enterocolitis resembling human campylobacteriosis,254 triggering mixed Type1/Type17 cytokine responses where IL-17 suppressed bacterial survival in gut epithelia.255 Notably, IFN-γ+ ILCs (exhibiting ILC3-to-ILC1 plasticity) drovet T cell-independent colitis,256 while PI3K-AKT and MAPK pathways emerged as key pathogenic mediators.257–259