However, the enhanced mortality in control WT mice is significantly decreased in Reg1+/− mice, which we propose is due to increased type I IFN that modulates the inflammatory response enough to facilitate bacterial eradication and pneumonia resolution, and this model is supported by histological evidence as well as the observation that anti-IFNR1 blockade reverses the protection provided by Reg1 deficiency. The gene discussed is IFNAR1; the disease is pneumonia.