IFNAR1 and influenza: Given that IL-27 production was significantly decreased in IFNAR-deficient mice after influenza infection (Fig 3), we predicted that decreased IL-27 may be the significant mediator of enhanced clearance of secondary pneumococcal pneumonia observed in IFNAR-deficient mice, and determined whether IL-27 treatment could reverse the tolerance to secondary pneumococcal pneumonia in IFNAR-deficient mice.