IL25 and infection: Compared with WT mice, Il-17ra deficient mice displayed a higher burdens of S. aureus in the brain; the influx of γ and δ T cells was increased in Il-17ra deficient mice following S. aureus infection; subsequently, the high infiltration of natural killer (NK) cells were absent in the brain abscesses in Il-17ra deficient mice, implying that IL-25 signaling played an important role in the regulation of adaptive immunity with the infection of S. aureus (116).