Critically, IL-22 and IL-17 form a synergistic axis: IL-22 deficiency amplifies IL-17-driven inflammation, whereas IL-22 supplementation restores bacterial clearance and attenuates inflammation (167)―This axis is vital during acute exacerbations, where bacterial infections (e.g., Streptococcus pneumoniae) cause delayed clearance due to IL-17/IL-22 defects, while viral infections (e.g., influenza) suppress their secretion by inhibiting IL-1β/IL-23, raising secondary infection risks (168). This evidence concerns the gene IL17A and influenza.